Neurology Clerkship UWORLD

Neoplasms
Epidemiology; median age 60, will have unilateral or bilateral associated with NF
Clinical manifestations; there is sensorineural hearing loss and inbalance (VIII) and facial
numbness/paralysis
Diagnostics; this will be done with audiogram and MRI with internal audatory canal
Management; observation, surgery and radiation
- Assymetric sensorineural loss; this will have air conduction, bone conduction and
lateralization with facial numbness----

CNVIII; this will be composed of cochlear nerve and vestibular nerve; inbalanece can occur and
it wil involve numbness due to CN VII involvement

Hydrocephalus; Choroid Plexus Papilloma;

This will be associated with ventriculomegaly; there will be an intraventricular mass-----CP
papilloma; this is a highly vascularized neuroepithelial tissue----there will be enlarged head
circumference; with increased ICP

Educational goal; choroid plexus paplilloma; there will be increased production of cerebrospinal
fluid and hydrocephalus; there will be enlarging head circumference and signs of elevated ICP.

Intracranial Tumour; there will be gait dysfunction, headaches with nauea worse in the
mornings with intracranial tumour affecting the motor cortex
- There will be nausea/vomiting, focal neurologic manifestations, and worsened
symptoms during the night (bending, coughing); there will show papilledema----
Diabetic polyneuropathy; there will be a sensory neuropathy of the lower extremity

Neuroblastoma;
Pathogenesis; this will be neural crest origin and it involves the adrenal medulla and the SNS
chain
Clinical features; median age <2, abdominal mass, periorbital echymosis, spinal cord
compression, opsoclonus myoclonus

Urine and serum catacholamines (VMA and HVA) are elevated, diagnose with tissue biopsy
Educational goal; neuroblastoma, this arises from the NC cells; precursors to the SNS ganngia
and adrenal medulla, it will arise in the cervical chain causing Horner syndrome

Pinealoma;
Clinical features; limited upward gaze, and upward eyelid retraction, pupillary abnormalities;
Obstrustive; papilledema, headache, vomiting, ataxia
 - There will be persistent headache ocuar abnormalities; concerning for pineal tumour;
this is localized to the quadrigeminal cistern and is responsible for melatonin
production---this will be in the prectectal region
- - there will be issues with upward gaze and light near dissociation and eyelid retraction

Paranaud syndrome; pineal gland masses----this is most commonly seen in children ; there will
be limitation in upward gaze; there is persistent gaze

Metastatic Tumours; Incidence---order of the increased metastatic brain cancer (lung? Breast,
and unknown primary tumour)
- Tobacco abuse; suggests metasatic spread; note that nneoplasms can travel-----this will
cause multiple lesions and present with seizures
Diagnosis; MRI ; will show well circumscribed lesions; glucocorticoids---this will reduce swelling
and palliate symptoms

Lung cancer; this is the most common neoplasm; it will metastasize to the brain; presents with
seizure and mental status change with well circumscribed lesions

Brain tumours; these are most consistent with a frontal lobe tumour; they can be asymptomat
Cholestoma; this will be keratin mass in the middle ear; it will be conductive, bone conduction>
air conduction
Eustachian tube dysfunction; assymetric hearing loss
HZV; can cause hearing loss but it will be linked to severe pain and vesicular rash
Menierre disease; this will have spinning vertigo, hearing loss and aural fullness
Educational goal; unilateral sensorineural loss will show reduced facial sensation. Vestibular
schwannoma, a benign tumour of CNVIII

Brain tumours; can be asymptomatic ---with ICP causes papilledema---cognitive dysfunction,

(unprovoked first seizure)
- Cognitive dysfunction (impaired memory)

Abuiia (motivation) and loss of interest (anhedonia)---there will be frontal lobe damage

FTD; this will manifest in the frontal lobe it is characterized by exective dysfunction-----
hereditary component most common ages 50-70

Educational goals; ICP and unprovoked first seizures are concerning for brain tumours; may
cause personality changes, abulia and anhedonia

Pediatric Brain tumours;

CNS tumours; this is the second most common subset of pediatric malignancies; this is a
common pediatric soft tumour origninating at the cerebral cortex;
 - New onset seizure; this may be the presenting symptom; there will be changes in
speech, memory and personality; hemiparesis and hyperreflexia;
Most common type of bran tumour; low grade astrocytoma;

Craniopharyngeoma;
Benign tumours; pituitary adenoma, craniopharyngioma; meningioma, pituicytoma
Malingnat tumours; germ, chordoma or lymphoma
Clinical presentation; this ca compress optic chiasm leading to bitemporal hemianopsia

Pituitary Apoplexy; she has severe headache, ptosis, and vision changes; there will be sudden
hemorrhage; without a clear precipitating cause; ----there is bleeding nnto the sella this will
cause bitemporal hemianopsia; eye dysfunction; and manifest in the pptic chiasm

Educational goal; pituitary apoplexy; sudden hemorrhage into enarged adenoma; will see
headache and visual disturbances; loss of pituitary function; absence of ACTH induced cortisol
leads to crisis; hypotension and distributive sock

Ischemic Stroke:

Risk Factors for ischemic Stroke:

Acute cerebral accident; this will have risk factors such as HTN, this will promote elevated
shearing force on the intracerebral vascular endothelium that will accelerate thrombi formation
- It will promote 4x the risk of CVA, even mild reductions in BP can diminish CVA risk

Less significant risk factors for CVA; HTN, smoking, and sedentary lifestyle
HTN; this will increase risk of stroke, more than other risk factors including
hypercholesterolemia, DM, smoking and a sedentary lifestyle

Ischemic Stroke;
Lateral medullary Wallenburg Syndrome; there will be seen in strokes; with the intracranial
vertebral artery distribution

- There will be spinning sensation, nanusea, and nystagmus; (sensation of the left side of
the face, and right extremities); there will be vertebral artery dissection
- There the loss of pain and temp; there will also be ataxia and nystagmus, dysphagia and
dysphonia and ipsilateral orner syndrome
Vertigo accompanied by loss os sensation of the ipsilateral face and the contralateral body (PCA
storke, precipitated by vertebral artery dissection post minor neck trauma

Lacunar strokes; < 15 mm in diameter; this will be cause dby occlusion of deep penetrating
branches; hypertensive vasculpathy (risk, DM< smoking, advanced age, and elevated LDL)

Acute unilateral infarct; without sensory deficits; this will be suggestive of lacunar storke in the
posterior limb of the IC:
Normal pressure Hydrocephalus;
There will be gait instability with frequent falls, cognitive dysfunction; urinary urgency and
incontinence; there is also depressed affect (frontal lobe compression). UMN signs in lower
extremities
Diagnosis; there will be marked improvement in gait with spinal fluid Millie Fisher lumbar test;
MRI
Treatment; VP shunting

Normal opening pressure on LP; there will be SAH; trauma, and destruction of the arachnoid
granulation that is responsible for CSF resoroption
Presentation; incontinence, cognitive impairment and gait abnormalities;

In sum, NPH is characterzed by ventriculomegaly with normal opening pressure, will show
incontinence, cognitive impairment and gait abnormalities in early disease; it is secondary to
neurologic insults that result in arachnoid granulations

Normal pressure Hydrocephalus;

THis is accumulationnn of CSF leading to ventriculomegaly; this will show normal opening
pressure there will be incontinence, cognitiveimpairment, magnetic gait; this will improve wth
large volume LP

NPH: this will be characterised by ventriculomegaly, normal opening pressure non LP: with triad
of incontinence; this can be secondary to nneurologic insults., SAH, trauma meningitis

Hemorrhagic Stroke;
Risk factors; Vascular malformations (AVMs), aneurysm,
Hemotological abnormalities (hemophaelia, SCD)
Clinical features; headache, vomiting, seizures, focal neurological deficits and AMS
Management; supportive, and reduction of ICP

HHT; this is concerning for an AVM; these are isolated congenital anomalous weakness through
weak vessels with telangectasia and multiorgan (lung, brain and liver); there will be sudden
onset of headache, vomiting, increased ICP

CT: shows irregular hyperdense region with margins

Repeat Hemorrhagic Stroke; there will be detoriation 2 days post ischemic stroke;
hemorrhagic transformation HT; this will be when the stroke affects a large area of the patient;
emergent noncontrast CT is key
- There will be treated with thrombolytics are at high risk for transport
Basal Ganglia Putaminal hemorrhage;
There will be BG putaminal hemorrhage, there will cause sudden focal neurological deficits that
worsen over minuts to hours; there will be affecting the adjacent internal capsule leading to
contralateral hemiparesis and hemianesthesia----as the hemorrhage expands; there will be
nausea/vomiting due to elevated ICP
- Hypertensive vasculopathy involves the small penetrating branches---leading to
formation of Charcot Bouchard

Lobar/cortical hemorrhage---this is the most common cause of lobar heorrhages in the elderly
SAH: there will be ruptured berry aneurysms; with thunderclap headache and hyperattenuation
Epidural hematoma; this will have head injury----Altered consciousness; headache, n/v

Educational goal

ICH; there is headache, nausea, vomiting and reduced likelihood of consciousness

- There will be AVM; this will be when the artery directly anastomosis into the vein;
capillary bed is interposed; other symptoms are recurrent headache

CAA; and hypertensive vasculopathy

Lacunar Stroke;
There will be in the internal capsule; there will be due to occlusion of the deep penetrating
arteries in the brain; the vessels are highly turbulent and are most susceptible to vascular
disease,
- Location; the internal capsule; ; there is risk of pure motor hemiparesisis;
Educational goal; lacunar strokes; this is due to microartherome; and lipohyelnosis in the small
penetrating arteries; they will affect the internal capsule; resulting in pure motor hemiparesis
- HTN, HLD, T2DM and smoking are major risk factors

Subarachnoid Hemorrhage;
Overview; this will show a hypertensive patient that is associated with a severe thunderclap
headache; meningeal irritation (nausea/vomiting—photophobia; they are also likely to suffer
from saccular//berry aneurysms

Management; this will be done with CT scan without contrast.

It will reveal acute hemorrhage in the brainstem and the basal cisterns with bleeding in the
intrahemispheric cistern and those with negative head CT will have elevated opening pressure
and xanthochromia

Cerebral amyloid angiopathy; this is the second most common cause of ICH; caused by
abnormal b-pleated sheets.

Aseptic meningitis; this will have headache, nausea. Vomiting, photophobia, nuchal rigidity
Cerebral venous thrombosis; this will be linked to hypercoagulable states with headache,
confusion and focal neurologic defects- diagnosis with venography

Vertebral artery dissection; causes local pain due to cerebral ischemia; this will be linked to
lateral medullary wallenburg syndrome; with ipsilateral Horner syndrome

Educational goal; nontraumatic SAH: due to ruptured saccular aneurysm and is linked to a
thunderclap headache and symptoms of meningeal irriaiton (nuchal rigidity, photophia and
nausea

Cerebellar Hemorrhage;
Patient has new onset neurologic deficits, confusion, medical history of vascular dementia,
HTN< and afib; this wil raise suspicion for stroke; this is an essential branch point
- There will be use of apixaban that can promote stroke; white hypedense

Subarachnoid Hemorrhage;
This will have a thunderclap headache (nausea, vomiting, photophobia, with SAH); this is
caused by a ruptured saccular aneurysm
Management; CT without contrast---this will cause blood deposition in the brainstem and basal
cistenrs;
Labs; reveal opening pressure and xanthochromia

SAH: this is caused by a rupture of a saccular aneurysm; this will be caused by a suden onset of
severe headache, thunderclap, this will be accompanied by vomiting and photophobia with
brief LOC; management, noncontrast CT scan of the brain; there will be xanthochroma

SAH; risk factors; HTN, smoking, moderate to heavy alcohol use, family history,
sympathomimetic drugs
Clinical presentation; this is most commonly due to a saccular (berry aneurysm),
nausea/vomiting, brief loss of consciousness, focal neurologic defects or meningmus
Diagnosis; noncontrast head CT ?90%, within 2-6 hours, xanthochromia confirms diagnosis and
cerebral angiography to identify the bleeding source
- Note that there is a thunderclap headache (meningmus), with uchal rigidity; this ma
manifest as a sentinel bleed; this will have a urgent noncontrast CT with negative LP

DDX; Cluster headache; this will be with ptosis, lacrimation and rhinorrhea;
Tension headaches; bilateral band like pain

In sum, SAH; sudden onset headache nausea/vomiting, brief LOC must do urgent noncontrast
CT with LP
Movement Disorders;
Parkinson Disease
Cardinal findings; bradykinesia, 4-6 hz testing tremor; or cogwheel rigidity
Suggest diagnosis; unilateral with craniofacial (mased facial expression, decreased eye blink,
visual (blurred vision and impaired upward gaze, MSK (micrographia, dystonia and myoclonus),
shuffling gait; stopped gait, postural instability, autonomic dysfunction, nonpsychiatric
depression, psychosis disturbed sleep and dementia

Recall; resting tremor, bradykinesia, and rigidity are consistent with PD; there will be
complicated psychiatric symptoms; this will have psychosis----
Management; pramiprexole and ropinrole will exasperate psychosis more than levodopa

DDx; Deliriub; this is an acute onset fluctuating disorder that occurs with medical illness,
pharmacologic intoxication or withdrawal
Dementia with Lewy bodies; REM sleep behavio, fluctuating cognition, parkinsonism

Educational goal; PD; will show bradykinesia, rigidity, and tremor with visual hallucinations.
Treatment is qith quietipaine and pimvaserin

Parkinson’s Disease Dementia;

Presentation, assymetric rigidity, resting tremor and bradykinesia; undiagnosed PD; this will
have risk factors such as age, duration and symptom severity
- There will be exclusive visual and executive disabilities (impaired attention/planning),
- Management; donepezil
Educational goal; PD; there will be executive and visiosspatial dysfunction with a mild memory
impairment; PDD should be diagnosed

Essential Tremor;
This will be associated with involuntary movements with a neurologic cause that improve with
distraction
- Functional tremor; this will have an abrupt onset and it will result in functional tremor
- Often spared
- Changeable; shifting tremor frequency----chase the tremor

Educational objective; psychogenic tremors; this will present with significant disability------
changeable or inconsistent features; not consistent with known tremor syndromes;

Tremor; THis is specially an inconsistent tremor with abrupt onset and cessation; it will be
abrupt onset and have functional disability out of proportion; It is reduced with distraction;
there are chanagable features

Functional/psychogenic tremors; this will be abrupt with significant disability; there will not be
considered known tremor syndrome
Spinal Cord Diseases
Spinal cord compression; there will be loss of sensation and signs of upper motor neuron
disease. Epidural abscess is a particular concern in the IV drug use community; there will be
UMN signs

DDx; Malignancy
Educational goal; spinal cord compression is a sign and symptom of UMN disease, includes
weakness, hyperreflexia and extensor plantar response.

Spinal Cord Compression

Causes there wll be associated with spinal injury; malignancy, (lung, breast, prostate, and
myeloma; infection---epidural abscess), there will be pain worsened at night; early signs absetnt
DTRS

SCC: there will be associated by malignancy there will be progressive back pain, manifestation
with 6-8 weeks. Immediate neurosurgical evaluation is done
- Acute spinal cord compression, presents with loss of motor and sensory function; loss of
rectal tone with urgent surgical consultation

Spinal Cord Compression;

This is associated with spinal injury; MVA, malignancy, (lung, breast prostate, myeloma)
infection (epidural abscess)
There will be pain that gradually worsens, severe low back pain; it will worsen at nnight; early
signs, lower extremity weakness; hypoactive DTRs, late signs, bilateral Babinski;
Management; emergency MRI, IV glucocorticoids vs. antibiotics

Prostate cancer; subacute back pain, lower extremity weakness, hyperreflexia, bladder
dysfunnctionn shows spinal cord compression (Thoracic, lumbosacral 30%), there will
metasisize to the spine, lung, breast and prostate
- IV glucocorticoids; for suspected ESCC
Epidural spinal cord compression; any history of malingnany with motor and sensory
abnormalities, bladder and bowel dysfunction----are late findings

Radiculopathy;
There will be sudden onsetof low back pain that radiates to the left leg, it is associated with
sensory and motor deficits; this is due to L5 nerve compression;
Clinical presentation; low back pain; there will be pain and sensory loss involving the buttocks,
lateral thigh and calf
- This will manifest in a dermatoma and myotomal distribution; there will also be
weakness (potential atrophy); foot dorsiflexion and innversionnn
Educationnal goal; L5 radiculopathy, this will present with low back pain, this will be associate d
with sensory loss over the lateral thigh, calf and dorsal foot
Spinnnal Cord Compression; this is common in older adults with spinal cord narrowing; there
will be LMNN findings (weakness, atrophy reduced reflexes) and damage to SC; this will lead to
UMN signs
- There will also be positive Lhermitte sign;
Educational goal; cervical spondylotic myelopathy common in older adults with progressive
neck/gait disturbances

Cervical Spondylosis; this will manifest with upper extremity weakness, reflex loss, and
incomplete acute spinal cord injury
- There will be hyperextension injury to the necl; this will compress the spinal cord
between the hypertrophied ligamental flavum---there will be primary upper extremity
manifestations; weakness to the damanged UMN

Central cord syndrome; this will be post whiplash type injuries; in oder adults- underlying
cervical spondylosis

Back Pain; Spinal Disease;

Overview; back pain is common and should be benign; in children; back pain is often due to
spondylolisthesis; this will represent the pars interarticularis; this will have a forward slippage
of L5; it is most common in adolescents

Pathogenesis; atheletes with repeated extension and rotation, there will be a palpable step off
during the exam

Spinal Cord Injury;

There will be findings such as altered sensorium, quadriplegia; consistnet with cervical spinnne
trauma; begin evaluation with primary survey (ABCDE) ;

Anterior cord syndrome; this will have loss of pain/temperature and bilateral paralysis; there
will be disruption of ANS tracts involved in bladder control

In those with traumatic spinal cord injury disruption leads to urinary retention; catherization
should be done to avoid bladder distension and injury

Anterior Cord Syndrome; this will be caused by injury to the anterior spinal cord (disc
retropulsion, fragments of the bone from the vertebrae and at the anterior 2/3 of the spinal
cord
- There is bilateral hemiparesis; lateral corticospinal tract---
- Diminished bilateral pain and temp sensation
- Intact proprioception, vibratiory sensation and light touch
Educational goal; anterior cord syndrome; injury to the ACA from trauma; bilateral motr
function loss below the lesion with diminished pain and temperature sensation
Friedrich Ataxia; AR with CGG repeats; there is elevated abnormalities of frataxin; this is
expressed in the brain, heart and pancreas
- Neurologic dysfunction, cardiomyopathy, and DM
- There will be loss of proprioception in the dorsal column
ALS: there will be asymmetric muscle strength, music atrophy, early resp insufficiencny; there
will be both UMN and LMN weakness;
- There will be diaphragm atrophy, poor inspiratory strength, ineffective respiration,
NPPV this will improve resp function, opening upper airay, positive PEEP: improves
atelectasis; this is the first line treatment for ALS; it can be used intermittmently at night

ALS: there will be resp insufficiency; resp musclw eakness, with NPPV prolonging survival and
improving quality of life

ALS: there will be both UMN and LMN dysfunction, hyperreflexia (atrophy and fasiculations)<
this is due to ALS (there will be elevated CK)
- There will be fatal, therefore the management is focused in slowing progression
(glutamate inhibitor); this will show excitotoxicty \there will use this edaravone
(antioxidant)

ALS: this will be implicated in UMN and LMN signs, management is with riluzole and edaravone

Transverse Myelitis;
This is an ummune mediated destruction of the spinal cord, often postinfectious (molecular
mimicry); bilateral motor weakness, early flacid paralysis, late spastic UMN)
Diagnosis MRI of the spine, T2 hyperintesity; LPS elevated WBC and elevated IgG index
Treatment; high dose IV glucocorticoids; plasmapheresis

Rapidly progressive myelopathy; this has weakness, sensory dysfunction and autonomic
dysfunction;

Transverse Myelitis; this will show UMN signs with urinary incontinence; this will have
infiltration of inflammatory cells into a segment
- There will be motor weakness, autonomic dysfunction and sensory dysfunction
including pain, paresthesia with a distinct sensory level
- Management high dose IV glucocorticoids
Transverse myelitis; this is an immune mediated disorder characterized by inflammatory cells
>1 contigious spinal cord segments with sensory defects with a distinct sensory level

Autonomic Dysreflexia;
C6 paraplegia; this will cause severe HTN, diaphoresis, flushing and bradycardia in the setting of
urinary retention suggesting autonomic dysreflexia
- This will be modulated by higher level ANS neurons;
SCI; the modulating pathways are disrupted below the lesion; it will cause bradycardia and
vasodilation, below there is an unregulated SNS response

Educational goal; Spinal cord injury above T6 complicated by ANS dysreflexia; in which noxious
stimuli below the lesion triggers an unregulated response; this will be managed by removing
noxious stimuli

Cervical Radiculopathy
The patient has pain in the right shoulder ; this will involve the c6 root and this can cause
radiculopathy due to compression of the C6 nerve root; this will be caused by repetitive action
and will manifest following repetitive exercise; golf;
- There is pain in neck; associated with sensory/motor defficits
- Mannage with NSAIDS
In sum, cervical radiculopathy; caused by nerve root compression due to disc herniation or
spondylosis; includes neck pain, shoulder/arm pain, weakness and paresthesia;

Spinal Cord Compression;

Causes; spinal injury; (MVA), malignancy (breast, lung prostate and myeloma)
Infection (epidural abscess)
Signs/symptoms; there is worsening severe low back pain it is worsened at the recumbnent
position at night; Early signs, symmetric lower extremity
- There will be worsening back pain the recumbnent position, there will be lower
extremity weakness, fecal or urinary retention with exaggerated DTRS
Location; in this case we can localize to T8;

Educational goal; epidural spinal cord compression, presents with worsening focal back pain,
bilateral lower extremity ataxia with bladder and bowel disturbances; there will be increased
reflexes and flaccid paraplegia

Spinal Cord Compression;

DM; this will cause back and leg pain; ddx; this will cause a stocking and globe neuropathy, with
decreased ankle reflexes; hyperactive knee jerk and positive Babinksi sign;
- However because of UMN signs; it may be a a mass that is causing compression
-

Cervical Myelopathy;
Epidemiology; age > 55, there is degenerative cervical spine/discs/canal stenosis and
compression
Manifestations; there is gait dysfunction; usually first, then there is extremity weakness and
numbness
- There will be spondylosis of the cervical spine that is diagnosed radiographically and
myelopathy is confirmed with CT/MRI; requires a surgical decompression
Educational goal; the most common cause of cervical myelopathy is spondylosis; this is a
dengenerative spine disease causing spinal cord compression; there is progressive gait
instability and weakness of the extremities;

Epidural Abscess:
Pathogenesis; this will be caused by staphylococcus aureus
- Thi will be a distant infection (cellulitis, joint/bone pain), or IVDU
- Classic triad; fever, focal severe back pain and neurologic findings (motor sensory loss;
bowel or bladder dysfunction and paralysis

Overview; there will be worsening focal back pain, radcular nerve pain, sensory motor or reflex,
and paralysis

Suspected cases; urgent spinal MRI to confirm diagnosis followed by surgery---this can have
neurological sequelae and death

Spinal Epidural Abscess

Epidemiology; staphylococcus aureus; it is associated with distant infection, cellulitis,
joint/bone involvement along with IVDU
Manifestation; fever, focal severe back pain and neurological findings
Diagnosis; elevated ESR, blood and aspirate cultures and spinal MRI
Treatment; broad spectrum antibiotics (vancomycin and ceftriaxone)

- SEA; this will result in a triad of fever, back pain and neurological defects; however, they
will all develop severe focalized back pain that progresses through a series of days

Spinal epidural abscess; this will present with focal back pain and neurologic dysfunction; there
will be treatment required with broad spectrum IV antibiotics and prompt drainage/surgery

Spinal Cord Compression;

Spinal injury; MVA, malignancy; infection
Signs/symptoms; worsening severe low back pain that is worse at night and at the recumbent
position; there will be hypoactive or absence; late signs; bilateral babinksi reflex; decreased
rectal sphincter tone and increased DTRs
Management; emergency MRI; IV glucocorticoids

Central Cord Syndrome;

Cervical Cord spondylosis; there wil be acute spinal cord injury; with hyperextension and
collision
- There is commonly upper extremity manifestation including weakness due to damage of
the a- motor neurons in the anterior horn; there is also pain temperature and sensory
loss. There is also reflex loss at the level of injury
Educational goal; central cord syndrome, this is post whip lash injury in older adults with
underlying central cervical cord causes upper extremity, motor, sensory and reflex abnormality.
LMN function is generally preserved

Idiopathic Transverse Myelitis;

Pathophysiology; this will be immune mediated destruction of the spinal cord;
Clinical features; bilateral motor weakness, clasicially early flaccid
Distinct sensory level; autonomic dysfunction
- There is motor weakness with UMN signs and sensory dysfunction; rapidly progressive
with UMN and LMN signs characterized by distinct sensory loss; bladder dysfunction

Syringomylia;
Pathogenesis; this is adisoder in which a cavity forms in the spinal cord, this will cause a cavity
in the spinal parynchma; there will also be dermatomal involvement with capelike distributionl
with dissociated sensory loss
- Continued syrinx involvement will form disproportionate weakness in the upper
extremity
Dorsal column pathway; this will reduce vibratory and proprioceptive sensation
Anterior cord syndrome; loss of pinn and temp below spinal level

Peripheral Neuropathy
Metabolic; diabetes mellitus, hypothyroidism, vitamin B12
Toxic; alcohol use, medications (phenytoin, disulfram, platinum
Heavy metals
Infection; HIV and lyme disease
Hereditary; CMT and porphyria
Other; idiopathic, plasma cell disorders (MM or MGUS)
- Note that excessive alcohol intake is neurotoxic and axonal neuropathy; will occur
association with the thiamine deficiency resulting in a symmetric distal polyneuropathy
Educational goal; alcohol neuropathy; toxic neuropathy; this will result in a distal
polyneuropathy; with paresthesia, burning and ataxia; with loss of DTRs and light touch

Common fibrillar Neuropathy;

Note the common fibrillar nerve travels near the fibrillar head and is susceptible to
compression injuries
- There will be unilateral foot drop, numbness tingling over the dorsum and lateral shin,
impaired dorsiflexion and preserved plantar flexion

Common fibrillar neuropathy; this is a result of leg immobolization, protracted squatting and
sensory changes over the forsal foot and lateral shin
Guillain Barre Syndrome;
Pathophysiology; this is an immune mediated demylenating polyneuropathy; preceded by
campylobacter or resp infection, ther eis paresthesia, neuropathic painnn, decreased or absent
DTRs, resp compromised; managementl ANS; resp function – diagnosis made with LP; GBS
management includes supportive care monitoring ANS and resp function

GBS; this is characterized by ascendingweakness, bulbar symptoms and resp compromise with +
albuminocytogenic dissociation

Dementias
Alzheimers Disease; there is early, insidious short term memory with language deficits and
spatial disorientation. There is also personality
changes;
Vascular dementia; there is a stepwise decline, early executive dysfunction, cerebral infarction
FTD; there is early personality changes, apathy and compulsive behaviour
Dementia with Lewy Bodies; visual hallucinations, spontaneous Parkinsonism, fluctuating
congition and rapid eye movement with sleep behaviour disorder

NPH; there is ataxia in early disease, urinary incontinence, and dilated ventricles on
neuroimaging

Alzheimers Disease; this will show decreased daily functioning with prominent memory loss and
reduced executive functioning with temporal lobe atrophy (seen in later stages)

AD: this will present with memory impairment with temporal lobe atrophy localized inn the
hippocampi and the medial temporal lobes

Alzheimers Disease;
Most common form of dementia; this will have modifiable risk factors; such as HTN, diabetes,
encouraging weight loss and increased PE
- Maintain social relationships and cognitive activity are critical for AD

Educational goal; FH of AD; increased risk of developing disease; but it can be mitigated
byaddessin risk factors for disease; Educational goal; those with family history of AD are at
increased risk of developing disease but can mitigate risk factors by addressing modifiable risk
factors *HTN, diabetes, obesity/physical activity)

Prion disease; behavioural changes, rapid progression, myoclonus and or seizures

Behavioural changes; this includes socially offensive behaviour, social withdrawal, and
hyperorality (apathy, lack of insight)
- There is a behaviour variant FTD
ALzheimers Disease;
 - Alzheimers Disease; this will have early onset insidious short term memory loss; there
will be later personality changes
- AD is the most common cause for dementia; begins with memory loss for recent events;
with psychotic features that manifest in the middle and late course of the disease;
vascular dementia; pseudodementia; cognitive changes

Educational coal; AD; this is the most common cause for dementia; characterized by insidious
memory loss followed by behavioural changes, psychotic symptoms will develop later in the
disease course

Prion Disease;
Clinical features; this will have rapidly progressive dementia, myoclonus, cerebellar signs, UMN
signs such as hyperreflexia, and extrapyramidal signs such as hypokensia and mood.sleep
disturbances

Findings; will show widespread atrophy of the cerebrum and cerebrullum, cortical
enhancement of the putamen and caudate/hocky stick sign
CSF: 14-3-3 protein and positive RT-QUic PCR
EEF; sharp triphasic synchronous discharges

Periodic sharp wave complexes; will have CJD; thre will be neurodegeneration and widespread
loss of neurons. There will be inexorable decline (loss of speech, loss of ability of self care less
than 12 months post diagnosis

Educational goal; CJD; this is a fatal prion disease with rapidly progressive dementia,
myoclonus, sleep disturbances, there is no effective disease modifying treatment

CJD; There will be caused by prion; this will have rapid onset neuropsychiatric symptoms

Prion Disease; there will be rapidly progressive dementia; startle myoclonus; mood symptoms
such as depression and hypersomnia; there will be elevated 14-3-3 protein, elevated tau, and
no WBCS
- RT-QPCR; performed on the CSF; can allow us to detect prions even better

DDx; anti-hu; this is with SCLC;

Anti-NMDA; there will be associated with ovarian teratoma
Narcolepsy; low levels of orexin, hypocretin; excessive daytime sleepiness;

Vascular Dementia;
There is a stepwise decline with early executive dysfunction, cerebral infarction or deep white
matter involvement; there will be ischemic changes detected upon neuroimaging
Dementia; this is MND; this a progressive cognitive impairment in ADLS: there will be
neurological findings (assymetric reflexes, urinary frequency and gait disturbances
- VSD; note large artery infarction; cortical type VaD; i.e. MCA; stepwise decline

VAD; this is a large and small artery ischemia characterized with focal nneurological changes;
patients require neuroimaging

Frontotemportal Dementia; this willhave the behavioural variant, or Pick disease will cause
focal degeneration of the frontal and temporal lobes; will manifest with early personality and
behavioural changes, compulsive behaviours and executive dysfunction \- this will have earlier
onset than other dementing illnesses (usually in 50s); this must be differentiated from AD

Behavioural variant of FTD; early personality changes, dysfunction and memory difficulties that
develop later in the disease course; this will cause early age of onset

Frontotemporal Dementia;
Overview; there there will be socially offensive behaviour, compulsive behaviour and
hyperorality with executive dysfunction (Difficulty with planning)
- FTD; presents around age 60, affects men and women at equal rates; follows an
autosomal dominant pattern of inheritance; the degenerative process is more rapid;
Behavoural variennt

Lewy Body Dementia; this is characterized by visual hallucinnations, spontaneous

Parkinsonism; fluctuating cognition and REM,
- There will be low MOCA assessment and 2/4 additional core features
- Parkinsonism (limb rigidity), fluctuating congition, visual hallucinnations, REM sleep
behaviour disorder

Lewy Body Dementia; there will be confusion, memory loss prominannt visual hallucinations;
REM Sleep behaviour disorder and Parkinsons disease; there will be elevated sensitivity to
antipsychotics; supportive clinicial diagnosis; i.e. Haldol

In sum, there will be fluctuating cognitive impairmetnt; recurrent visual halluciations; REM
sleep behaviour disorder;

Delirium;
Predisposing risk factors; dementia; PD, prior stroke, advanced age, senory impairment
Precipitating factors; drug, infection, electrolyte disturbance, metabolic derangement,
ssystemic illness, and CNS dysfncion

In sum, delirum; acute confusional state with reduced or flucutuating level of conciousess;
along with anxiety agitation and hallucinations; infection, medication side effects and metabolic
disturbances
Headaches
Migraine; there will be abnormal activation of trigeminal nerve; triggers, sleep deprivation;
stress and menses; epidemiology; increased incidence in boys and irls until puberty

Migraine with Aura;

This will manifest with recurrent unilateral headaches linked to nausea and paresthesia; this is
called migraine with aura; it is an episodic neurological disorder with photophia,
nausea/vomiting; more frequently in women than in men
- There will be increased risk of ischemic stroke with estrogen and progesterone pill

Educational goal; migraine is an episodic neurologic disorder; severe, unilateral throbbing pain
with photophobia, phonophobia nausea and vomiting there is a aura that precedes headache

Migraine in Children;
Equal incidence in boys and girls until puberty; there will be a raised risk in adolescent girls;
Clinical features; there is associated photophobia, nnausea/vomiting---autonomic symptoms
(facial sweating with precending aura), there is a normal nneurological exam
Abortive treatment; there will be managed with NSAIDS

Overview of the migraine; this will be episodic unilateral throbbing pain consistent with a
migraine (CGRP) is released---this is a neuropeptide released with fasting, dehydration, menses
—episodic unilateral headache; photophobia

First line; lying down in a dark quiet room;

Migraine;
Pathogenesis; there will be abnormal neuronal activation of the trigeminal ganglion; trigger is
sleep deprivation, stress, menses, fasting
Epidemiology; there will be an equal incidence in boys and girls until puberty- increased risk in
adolescent girls and women
Clinical features; throbbing headache, hours to days increased incidence in girls and women
- There will be a normal neurological sensation
Trigges; this includes sleep deprivation, stress menses---there will be a throbbing and pulsatile
quality;

Migraine Management;
Abortive therapy; triptans, NSAIDS, and acetaminophen, antiemetics and ergotamine
Preventatitive; anticonsulvants, b-blockers and antidepressents
- Note migraine headaches are common in the child bearing woman due to cyclical
changes in estrogen and progesterone, there is an increased in risk factors such as sleep
disturbance, physical exertion and emotional disturbance
- Frequent migraines with significant impairment that will benefit from preventative
therapy

Cluster Headache; there is acute, severe, right periorbital pain; associated with miosis,
lacrimination but no visual changes; this will be rapidly acting----effective abortion of cluster
headache; with 02

Presentation of the cluster headache; begins during sleep; peaks rapidly; and lasts
approximately 90 minutes and occurs over weeks

DDx; carbamazepine; this will be used to manage the trigemninal neuralgia; it will be along the
V2/V3-
Temporal arteritis; > 50, elevated ESR-----manage with glucorticoid; hyperglycemia
Educational; goal; 100% 02 by facemask is an effective and rapid method to abort an acute
cluster headache

Cluster Headache; This will be characterized by acute left retroorbital pain; with ipsilateral
autonomic symptoms; this is seen inn young men, with tearing; there will be beginning during
sleep, peak rapidly manage with 100% oxygen;

Differential; acute maxillary sinusitis; there will be facial pain and rhinorrhea---
Acute closure glaucoma; this will present with sudden onset eye pain, nausa
Migrans; this will show with nausea, bomitinng, photophobia;

Retinal detachment; this will present with light flashes or a curtain;

Cluster headache; this will be a acute unilateral retrobital pain; this will be associated with
redness, tearing, rhinorrhea, ptosis and miosis

Opthalmology
CMV retinitis; This will be followed by a latent lifelong infection; there will be severe deficits in
cell mediated immunity due to the loss of CD4+ cells, < 100, there will be blurred vision, floaters
and photopsia;

Fundoscopy; will reveal yellow fluffy hemorrhaegic lesions

Management; valganciclovir; this will reduce risk of blindness and retinal detachment
Antiretroviral therapy should also be initiated
Educational goal; CMV retinitis; this is the most common end complication of CMV int hose
with advanced AIDS, there will be blurred vision, floaters and photopsia (sensation of flashing
lights), there will also be retinal detachment; treatment necessitates antiretroviral medication
to prevent recurrrance

Age Related Macular Degeneration; AMD: this is seen in patient’s > 50, it will present with loss
of central vision; peripheral fields and navigational vision are normal; - there will be deg
- There will be seen in patients > 50, it will cause progressive weakness with preservation
of navigational vision

Open angle Glaucoma; there is vision impairment when receiving glucocorticoid eye drops;
this will lead to open angle glaucoma; we will manage with glucocorticoid eye drops and
systemic glucocorticoids; this will raise IOP due to decreased drainage in the anterior eye
chamber
- Note that open angle glaucoma; this will be characterized by insidious loss of peripheral
vision relating to atrophy of the optic disc/cup; note that steroid induced OAG can cause
central blurriness and edema---measurement; tonometry

Educational goal; topical glucocorticoiud; this can raise IOP and lead to OAG; this will have
insidious loss of peripheral vision and some patients have central blurriness due to corneal
edema. Measure with tonometry

Optic Neuritis;
Epidemiology; this will occur primarily in young women and is associated with MS; there is
immune mediated demyelnation, manifestations; acute peaks at about 2 weeks, with
monocular vision loss, eye pain with movement, afferent pupillary defect
Treatment; IV corticosteroids;
- There will be a central scotoma
Optic neuritis; this is associated with multiple sclerosis; it is the heraliding symptom of this
condition, able to look at other areas of inflammation

CRAO: this will cause acute, severe, painless monocular vision loss;
Cortical blindness; this will cause total loss of partial vision

Retinitis Pigmentosa;
Etiology; genetic mutation causes loss of photoreceptors; there is progressive retinal
degeneration, symptoms onset from age 10 through adulthood
- Clinical features; night blindness, progressive visual field loss decreased acuity
- Fundoscopy; this will be retinal vessel attenuation
Prognosis; most are legally blind by age 40;
This will cause peripheral vision loss and scotomas (degeneration of cones, photoreceptors on
the central retina; fundoscopy will cause retinal vessel attenuation, pale optic disc in a bone
spicule like pattern;

- This will cause progressive degeneration with peripheral vision loss; causes retinal
pigment deposition attenuation and pallor

Obstetrics and Gynecology;

Risk factors; inherited thrombophilia, protein C/S deficiency, factor V; there is also association
with pregnancy and post partum; OCPs, malignancy and infection
Clinical; headache, elevated ICP (vomiting, and papilledema), seizures, and encephalopth
Diagnosis; MRI of the brain with venography
Treatment; anticoagulation (heparin acutely)

Pregnancy; headaches are typically benign; acetaminophen first line option

Central venous thrombosis; this is a rare life threatening formation within the dural sinuses, it is
related to a prothrombotic state including inherited thrombophilias; it will obstruct dural
venous drainage from the blood brain barrier.
- It will manifest with elevated ICP and seizures, vomiting and headache worsened in the
morning
- Management; MR venography that will help visualize flow deficit
Central venus thrombosis; prothrombotic conditons (postpartum, elevated ICPs, seizure and
stroke; will be confirmed by viewing flow void or MR venography

Urge Incontience
Micturition Centers;
Cerebral cortex; it will maintain continence by blocking urination
Pontine micturition center; coordinates detrusor contraction

MS: this can cause urgency incontinence; there wil be impairment of the UMN (descending
corticospinal tracts are inhibited leading to a micturition reflex and a small overtly contracted
bladder;
Management; antimuscarinics
In sum, those with MS can manifest with urge incontinence due to loss of cortical inhibition.

MS; patient has neurological defects; this will cause dissemination in space/time, including
trigeminal neuralgia; spastic lower limb paralysis; and this will make a diagnosis of MS more
likely
Educational goal; MS; is suspected MRI is not classic this will show oligoclonal bands

Preeclampsia
Risk factors; nulliparity, obesity, pre-existing medical conditions such as SLE, chronic HTN,
multiple gestation and advanced maternal age
Definitions; there will be new onset HTN (SBP > 140, or DBP > 90 at > 20 weeks, proteinuria or
signs of other end organ damage

Management < 37 weeks and no severe featuees; expectant, > 37weeks delivery
PO Nifedipine and seizure prophylaxis with magnesium sulfate
- There will be a unilateral frontal headache, visual aura, vision loss; this will also have
HTN SBP > 140, DBP >90, can have severe features
BP; will cause acute elevations in dysregulated cerebral blood flow; management labetolol

Educational goal; preeclampsia with severe features > 20 weeks with SBP > 140, and DBP > 90
with vision changes (blurry vision)

Eclampsia;
Clinical features; HTN, SBP > 160, DBP ? 110, there is seizures, tonic clonic with post ictal state,
severe headache, visual disturbances; hyperreflexia and proteinuria
Diagnosis; these are mainly clinical; with bilateral frontal lobe edema
Eclampsia; this is a clinical based diagnosis; there is bilateral frontal or occipital lobe edema----
eclamptic seizures can raise risk for stroke

Management; this is done with IV magnesium sulfate, treatment with fetal delivery
Eclampsia; generalized tonic clonic seizures, can develop with preeclampsia, there is elevated
creatinine with post ictal state and persistent headache. Manage with magnesium sulfate
infusion

Psychiatry
Extrapyramidal Symptoms; Patient presents with worsening restlessness, wandering and
inability to sit still; this is suggestive of akathisia---there will be an inability to sit still; especially
in those with dementia who have limited verbal communication;
- Step 1 in management; dose reduction test; drug choice, propranolol or benzodiazepine
trial; if antipsychotic cessation is not an option; then a different antipsychotic
medication should be used

Antipsychotic; this will treat behavioural disturbances but it can cause akathisia; this is an
inability to sit still; management; dose reduction trial

Ropinnrole;
This will cause new onset behaviour changes; it is a DA agonist; has a high affinity for D2; this
will cause impulse control disorder; the first step is to discontinue the offending medication
Ovarian Teratoma; this will present with anxiety, psychosis, insomnia, autonomic instability,
cognitive impairment, rigidity, dystonia post flue prodrome----this is called an Ovarian
teratoma; immunosuppression is often donne
- Anti NMDA encephalitis; AI encephalitis characterized by psychiatric symptoms; seizure,
ANS instability, (median age 21) with ovarian teratoma >50%

Pseudodementia; Overview; there is anhedonia, feeling--------There will be anhedonnnia;

impaired ability to think; *pseudodemennti; there will be compromised concentration, memory
and executive function; during cognitive testing, patients will exhibit reduced memory,
concentration and executive function

Management; SSRI;

Depression related cognitive impairment; so severe in the elderly; the psychotherapy is a

treatment of choice for cognitive reversal

Akathesia;
Overview; the patient manifests with worsening restlessness, wandering, inability to stand still;
akathisia; this is an extrapyramidal condition; associated with high poetency antipsychotics;
Management; dose reduction trial and discontinatuon of antipsychotic medication.

- This will treat behavioural disturbances in dementia; management; dose reduction trial
and antipsychotic medication

Conversion Disorder; (functional neurological symptom disorder)

Clinical features; neurological symptoms; weakness, paralysis, nonepileptic seizures---not
intentionally produed (contrary to factitious disorder or malingering
Symptoms cause severe functional impairment and its precipitating
- This will be caused by relationship conflicts; or other stressors and support for patients

Pseudodementia; In this we will see increasing forgetfulness, low energy, sleep disturbance and
psychomotor retardation consistent with MDD; older patiennts may show cognitive impairment
and slowing rather than depressed mood; this will be reversible and improve by treating the
underlying dementia;

DDX; AD; this will be difficult to differentiate; but note that with ADH; there is no insight to their
condition
o

Antidepressents;
MDD; there will be MDD and worsening diabetic neuropathy; this is distressing and a disabling
complication that can exasperate depression, sleep disturbance and SNRI, duloxetine is shown
to have efficacy for depression and is the preferred choice in this patient

Educational goal; SNRI; duloxetine has analgesic properties for comorbid depression and
chronic pain and this includes painful diabetic neuropathy

CJD;
This will be a rapidly progressive dementia with myoclonus; cerebellar signs, UMN signs such as
hyperreflexia; extrapyramidal signs and mood/sleep disturbances
Findings; MRI; will reveal widespread atrophy; cerebellum and cerebrum
- MRI will show widespread atrophy (cerebrum and cerebellum; cortical enlargement and
caudate head---CSF 14-3-3 titers
- EEG; sharp triphasic synchronous discharges with spongiform degeneration without
inflammation

CJD: this will be an abnormal folded protein prion; this is promoted by startile with
noninflammatory neurodegeneration

RT-QIC tet can also be done

Prion Disease; CJD:

THis is a rapidly progressing dementia; this will present with myoclonus; provoked by startle,
cerebellar signs; UMN signs---extrapyramidal symptoms; such as hypokinesia; mood or sleep
disturbances; CJD; there will be rapidly progressive cognitive declie, personality channnnges,
cerebeullar dysfunction; CJD; this is caused by a prion; there will be noninflammatory
neurodegeneration
- There will be nonspecific 14-3-3- protein and elevated tau
Educational goal; CJD: this is fatal prion disease with rapidly progressive personalit changes,
visual cortex dysfunction, myoclonus; fluorescent labeled proteins are diagnostic

CKD; this is a fatal prion diseae with rapidly progressive dementia, personality changes visual
cortex degeneration, hypersomnia and myoclonus; fluorescent labeled proteins are the most
sensitive test

Medicine;
ESRD: this will have tingling, numbness and burning of the hands; suggesting CTS; there will be
compression of the carpel tunnel in the wirst; this is the most common mononeuropathy for
those on hemodialysis; this will be dialysis related; with increased venous pressure; blood
tracking; there will also be risk for ischemic neuropathy---note that symptoms worsen during
dialysis; it is reproducible with provocative measures

Educational goal; CTS; this is the most common mononeuropathy with ESRD with pain and
paresthesia; this will worsen during dialysis and more sever ein the arm with vascular access
Pediatric Stroke
Etiologies; SCD, prothrombotic disorders, congenital cardiac disease, bacterial meningitis,
vasculitis, focal cerebral arthropathy and head/necl trauma
Diagnosis; hemoglobin, electrophoresis
- Chronic vasooclusion; this will cause endothelial damage, intimal proliferation and
vascular steosis
- Confirmation; with MRI

TOdds paralysis; seizure will be followed with focal weakess that resolves within hours
MELAS: (mitochondrial myopathy; this wil have lactic acidos and stroke like episodes

Aminoglycoside Toxicity;
The patient is associated with gentamicin; there will be new onset hearing loss, inbalance
scillopsia (aminoglycoside), there will be associated with bacteremia, hepatic and renal
dysfunction----there will be damage in the hair cells of the cochlea (hearing loss)
- There will be bilateral hearing loss (positive whisper text requires formal audiogram
- Inbalance, oscillopsia (bilateral vestibular systems are affected)
- Positive head thrust test)---there will be immediate medication discontinationn
Multiple Sclerosis:
This is an AI disease of the CNS: there will be dissemination in space and disseminaton of time
in women 15-50, this will occur over hours; will show optic neuritis, transverse myelitis, INO
and cerebrallar dysfunction (intention tremor, ataia, and nystagmus)

DDx; ACA; this will cause contralateral leg weakness

DP: Glove and stocking distribution
GBS: progressive ascending muscle paralysis;
B12 deficienncy; this will lead to sCD of the spinal cord

Medication Overuse Headache;

This is a near daily headache, with acute headache medications; associated with migaine,
present for >3 months; there will be headache upon awakening; and quick rebound;
management, cessation of the culprit drug

IIH; this will be dignosed with elevated ICP during LP; this will occur in overweight individuals
SAH; will show high risk features, age > 50, fevers, and thunderclap headache
Educational goal; medication overuse headache, chronic near daily headache, regular use of
acute headache medications; there will be present on awakening, followed by rebound pain;
cessation of culprit medication

Carotid Artery Stenosis (asumptomatic)

Risk factors; HTN< smoking)
Managementl medical therapy, antiplatelet, statin and strict blood pressure control
Symptomatic; this will be associated with TIA; there will be managed with CEA
Asymptomatic; lower than 70 % manage medically

Educational goal; CAS; medical therapy, aspirin and statins;

Normal Presure Hydrocephalus; there will be recurrent falls, memory impairment (NPH), there
is also gait dysfunction; most pronounced feature (small steps broad based), urinary
incontinence and dementia; (hyperreflexia, spasticity and upgoing plantars

There will be ventriculomegaly (out of proportion to sulci on neuroimaging), management

placement of the VP shunt)

Wilson Disease;
Pathogenesis; AR mutation of the ATPB7 gene leads to hepatic copper accumulation in the
hepatocyte; Clinical findings; ALF, hepatitis, cirrhosis
Diagnnosis; decreased ceruloplasmin and increased urinanry copper
- Copper deposits in BG; leading to neuropsychiatric symptoms (Dysarthira, hyperreflexia,
and PD)
- Path; impaire dhepatobilliary cu transport
- Management; copper chelation
Wilson disease, hepatic, neurologic and psychiatric symptoms; increased urinary coper and
keyser Fleisher rings

Exertional Heat Stroke;

Risk Factors; Strenuous activity during hot and humid weather; dehydration, poor aclimitzaiton,
lack of physical fitnnness, obesity,
Medicaitions; anticholinergic, antihistamine, phenothiazinrs; antipsychotics

Clinical features; renal or hepatic involvement

Management; rapid cooling, ice water dosing, evaporative cooling, fluid resuscitation

Temp >40, this will have CNS dysfunction; need adequate fluids and removal from hot
environment; complications are DOC

Heat stroke; this is characterized with a temperature > 40 C, (104); with CNS dysfunction, most
commonly due to hot/humid environments; will have rhabdomyloysis, DIC and end organ
dysfunction

Increased ICP: headache, nausea, vomiting, MS changes with reduced LOC, cognitive
dysfunction; there will be vision changes, unsteady gait and seizure; (Cushing reflex—HTN<
bradycardia, resp depression; suggestive of brainstem compression;

Educational goal; ICH: headache, worse at night, nausea/vomiting, MS changes, papilledema,

and focal neurological deficits (HTN, bradycardia, and RDS suggestive of brainstem hemorrhage)
ALS Diaphragmatic Paralysis; there will be diaphragmatic weakness; ALS will show restrictive
pattern of disease (reduction in TLC), FVC, and MVP
- DLCO; remains normal because there is no restriction nor is there fibrosis
Educational; ALS, weakness of muscles of respiration, resulting in a restrictive pattern on
spirometry; reduced FVC and FEV1. DLCO is preserved

Delirium Management; there will be acute onset agitation and confusion with disorientation;
this will lead to delirium; this will occur in the elderly and those with underlying dementia;
- Delirum reversible disorder agitation and confusion, seen in the elderly with underling
dementia; encouraging regular activity----recovers more quickly

Brain Mass;
The patient has a migraine and it will be an infrequent, unilateral throbbing headache
- This is different than a headache on awakening (nausea, vomiting and blurry vision);
there will lead to consideration of early imaging
Neurologic findings; seizure, changes in consciousness, specific deficits
 40, sudden onset, trauma
Management; MRI
Headaches that differ from prior; associated with nausea and vomiting, evaluate with MRI

Sarcoidosis
This will cause new onset facial nerve palsy; bilateral gland swelling, hypercalcemia, and
constitutional symptoms; there is also risk for hular lymphadenopathy
- There will also be neurologic complications (granulomatous inflammation,) 10%
; there will be bilateral parotid gland swelling, hypercalcemia (1-a hydroxylase, lung
granulomas) and constitutional symptoms

Herpes Zoster Virus;

VZV from the geniculate ganglion (Ramsey Hunt Synndrome; reactivation of VZV,---there will be
a painful, erythematous rash from the auditory ganglion or auricle; management valcyclovir

Educational goal; RH; this will be caused by reactivation of VZV from the genu; disrupts cranial
nnerve VII: with spread to VIII: painfuerythemout rash

Acute Intermittment Porphyria;

Etiology; this is AD, low penetrance; reduced activity of porphilobillogen deaminase
Exacerbating actors; medications (CYP P450 inducers, progesterone)
Physiogic stress; (fasting, surgery, illness); alcohol and tobacco )
Manifestationsl abdominal pain, peripheral neuropathy, ANS dysfunction *tachycardia,
diaphoresis, psychosis)
Hallucinations, anxiety, and psychosis
Labs; elevated serum and urine PBG, ALA, porphyria
Management; glucose hemin
AIP: this is an AD disorder of the heme synthase pathway reduced porphobillogenn, leading to
heme toxins;
Peripheral NNS: proximal upper extremities, there will nnnot be be cutaneous findings;
hyponatremia is also present due to SIADH: diagnosis elevated protoporphyrin

AIP: this will cause reduced activity in porphobilinogen deaminase; there will be abdominal
pain, peripheral neirpathy, proximal muscle weakness, ANS dysfunction and neuropsychiatric
manifestations; elevated urinary porphyrin

Rheumatoid Arthritis;
Note that RA is associated with atlantoaxial joint instability; this will manifest in the small joints
of the hands; with elevated ESR, progressive erosive disease this can cause subluxation
(misalignment of the atlantoaxial joints; leading to cord compression and cervical myelopathy
- This will have UMN signs including Babinski sgnn; Hoffman sign; bending and flexing of
the thumb when flickinnng middle nfinger nail
Educational goal; RA; will be at risk for atlantoaxial instability; neck extension during intubation,
subluxation with cord compression and cervical myelopathy with slowly progressive spastic
paaparesis

RA; will be at risk for atlantiooaxial instability; neck extension during intubation with spastic
paresis involving the upper and lower extremities; hyperreflexia and positive Babinski sign

Wernicke Korsakoff Syndrome;

Associaed conditions; chronic alcoholism, malnutrition (anorexia); hyperemesis gravidarrum
- The pathophysiology; this will be thiamine deficiency, there will be ocularmotor
dysfunction with chronic malnourishment (short gut synnndrome)---there will be
thiamine involvement;

This will be associated with oculormotor dysfunction ; manage with thiamine supplementation;
this will be associated with confabulation---80% of patients with WE will develop Kosakoff
syndrome

Educationnal goal; there will be a neurological complication of thiamine deficiency; this will be
linked to long term alcohol use ; treatment is with thiamine

Subdural Hematoma;
Pathogenesis; this will cause rupture of bridging veins; risk factors; elderly and alcoholics,
infants,
- THis is supported by history of falls; this will cuse slow bleeding into the subdural space;
this will cause gradual sympotoms due to rupture of the low pressure blood vessels;;
noncontrast CT will show crescenntric shaped hypodensity

DDX; Cardioembolic stroke; this is when a left atrial thrombus dislodges and occludes cerebral
artery
Lacunar stroke; hyalinosis will lead to lacunar strokes (BG, thalamus, IC)
NH: this will cause gait difficulties, cognitive disturbances, and urinary incontiencne
Epidural hematoma; damage to the sphenoid bonne
Subarachnoid; this will have a thunderclap headache and a brief LOC
Diffuse axonal injury this is sheering and traumatic forces

Educational goal
Subdural hematoma; rupture of bridging veins, head trauma, risk factors advanced age, chronic
alcoholism; crescent shaped hyperdensity crossing suture lines
IIH: (idiopathic intracranial HTN);
The patients presentation suggests increased ICP, optic nerve sheath rsulting in swelling of the
optic nerve head that will be visualized as papilledema on exam;
- There will be a blind spot on the visual fields at the location such as those with
papilledema---this will be secondary to increased ICP
Amaurosis Fugax; this will be transient monoopthalmic vision loss (blindness in the ophthalmic
artery)
Cataracts; this will have gradual vision loss
Glaucoma; this will have increased IOp
Optic neuritis; this will be associated with MS

Amaurosis Fugax; there wil be painless, rapid, transient < 10 minutes of vision loss; there will
be suggestive of retinal ischemia due to atherosclerotic emboli from the ipsilateral carotid
arteries; there will be evaluated with duplex US

Amaurosis fugaz; this is is characterized by painless, rapid, transient monocular vision loss; tis
will create a curtain that descends over the visual field. Manage with carotid duplex

Subdural hematoma;
Acute subdural hematoma; this will cause tearing of the bridging veins; the use of
anticoagulents raises bleeding risk (leads to TBI)

Acute Glaucoma;
The patient has headache, nausea, blurry vision and sluggish pupil
 - This will be characterized by a sudden rise of intraocular pressure due to impaired
drainage of the anterior camber; this will be triggered by certain medications; this will
be precipitated by trihexaphenydul;
Educational goal; ACG; this is a vision threatening condition, associated with PD; it can arise
spontaneously; there will be sudden onset of severe glaucoma-----we need an urgent
ophthalmologic consultation;

Papilledma; this will be linked to increased ICP and have transient vision loss relative to head
position---there will be diagnostic evaluation, ophthalmic examination and persistent
papilledema can manifest with vision loss

IIH; Pseduotumour cerebri; this is in a young woman wth obesity; who has a headache
analogous; will have normal neuroimaging and elevated CSF pressure; will need to optic nerve
sheath fenestration to prevent blindness

Huntingdons Disease; Clinical features; motor, choreha, delayed saccadic movement,

psychiatric (depression, irritability and OCD) cognitive, executive dysfunction
Findings; genetic AD< neuropathology, loss of Gabaergic nneurons and imaging will show
caudate nucleus
Management; treatment is supportive and survival is 10-20 years

Cognitive dysfunction; psychiatric symptoms, chorea (abrupt jerking movements, delayed

saccades, motor impersistance and HD;; associated with depression, irritability, psychosis and
OCD
; Huntingdom disease; presents with psychiatric symptoms (depression, irritability and CAG
trinucleotide repeat with no DMARD

Huntingdon Disease;
Clinical features; motor, chorea, and decreased saccades
Psychiatric; depression, irritability and OCD
Cognitive executive dysfunction

Findings; Genetics; AD, CAG expansion disease

Neuropathy; there is loss of GABAergic neurons---caudate and putamenal atrophy is present

CAG; trinucleotide repeat expansion; putamen---caudate—this is preferently destroyed it is

- THis is associated with an anticipation effect in which the disease worsens with
generations

Critical illness Hypoxia;

Myoclonus; this is involuntary muscle contraction; this will be caused by prolonged hypoxia;
- MSE; this is an acute form of PMH; this will occur within 24 hours; it is a
generalized/symmetric myoclonus
- Lance adams; this is days to weeks post initial insult; focal and exasperated by action,
negative myoclonus

Myoclonus; this is sudden involuntary contractions or relaxation; acute form is MSE; this will be
symmetric myoclonus in the axial, limb and facial muscles; poor marker of prognosis

Acute Dystonia
Overview; there will be tortisolois; this is a focal dystonia; the contraction results in twisting,
repetitive movements or abnormal postures; can be congenital,idiopathic; secondary o
trauma/focal inflammation-----

DDx; essential tremor; this will affect the upper extremity; it will resolve in sleep and with
alcohol consumption
Chorea; this will have brief irregular and uninhivted movement
Athetosis; these are slow writhing movements that affect the hands
Tourette; this is involuntary stereotyped movements

Torticolis; this is a form of focal dystonia over the SCM; it is most likely medication related;
discontinuation will/may improve symptoms

Physiological tremor; this is an action/rest tremor; it is low amplitude hugh frequency; there
will be ennhamcement; with SNS (anxiety, caffeine)
- Fine action tremor; worsens with stress; low amplitude high frequency; enhance with d
symmetric; limited to hands
- Lithium toxicity; exasperates physiologic tremor;
- Management; hydration, haemodialysis

Wernike Korsakoff Syndrome

This is associated with chronic alcoholism, malnutrition, hyperemesis gravidarum; thiamine
deficiency
Pathophysiology; thiamine deficiency;
Clinical features; encephalopathy, oculomotor dysfunction, nystagmus, postural and gait ataxia
- There is encephalopathy, oculormotor dysfunction, nystagmus
- Postural and gait ataxia

There will be long term thiamine and B1 deficiency; there is a high rate of intake, therefore we
administer glucose before thiamine

In sum, thiamine deficiency will cause wenike encephapathy

-
Idiopathic Intracranial HTN:
Risk factors; obese women of childbearing age; medications such as retinoids, tetracycline sand
growth hormones
Clinical features; headache, vision loss, enlarged blindspot, pulsatile tinnitus, diplopia, and
papilledema
Diagnosis; neuroimaging, LP (elevated opening pressure)
Management; weight loss and acetazolamide,

IIH; this is most common in obese women of childbearing age; thee will be positional headaches
which raise ICP; pulsatile tinnitus will also occur, this will manifest as optic disc edema
- Diagnosis; with MRI; will reveal elevated opening pressure in the brain.
Educational goal; IIH; this is most common in obese women of childbearing age that will
present as pulsatile tinnitus, and papilledema; diagnosis is with MRI and then LP

Polyarteritis Nodosum;
Pathophysiology; underlying Hep B and C; there is fibrinoid necrosis of the arterial wall with
intimal narrowing and interal/external lamina damage with microaneurysms
Clinical features; fever, weight loss and malaise
Diagnosis; negative ANCA and ANA
Angiography; microaneurysm and segmental/distal narrowing with nongranulomatosis and
transmural inflammation; there will be mononeuritis multiplex; with underlying vasculitis;
- There is assymetric polyneuropathy

Skin involvement; livido reticularis; renal insufficiency and abdominal pain; there will be elev
ESR

PAN; this will have mononeuritis multiplex with ?2 noncontigous findings with skin renal and GI
manifestations with sparing of the lungs

Heat Stroke;
Risk factors; strenuous activity during hot and humid weather; there is dehydration and poor
acclimization, lack of physicial fitness and obesity is another risk factor;
Clinical featues, core temp > 40, organ and tissue damage is also present, DIC, coagulation and
ARDs
Management; rapid cooling in ice water, high flow old water, fluid resuscitation and electrolyte
correction, no rle for antipyretic therapy
EHS; this is a temp > 40, there is CNS dysfunction, nonexertional headt stroke; must remove
from hot environment
Complications are DIC, end organ dysfunction---management, ABCs, fluid resuscitation and
treatment of end organ dysfunction
Educaitonal goal; heat stroke > 104, with CNS dysfunction (hot humid enviornments when
performing extreme activites such as DIC and end organ dysfunction

Emergency Medicine;
This seizure behaviour is associated with forceful eye closure and absence of self injury
consistent with psychogenic nonepileptic seizure
- This will have forceful eye closure, rapid alerting, orienting and immediate memory
recall; this will manifest in crowds
Labs; there will not be associated abnormal cortical activity;
Diagnosis; video EEG

Psychogenic nonepileptic seizure; this will have forced eye closure side-side head/body
movement and post ictal confusion; the gold standard is video eeg which will not show
epileptiform activity

Seizures;
Presentation; there will be LOC; this is associated with a loss of postural tone (fall and
unresponsiveness) while in the shower---return to baseline mental status; the first time seizure
can occur at any age and can be unprovoked;
There will be < 3 minutes and will be unwitnessed aura will precede the event and a biting
event is common during the convulsion

Seizures, sudden LOC loss of postural tone, post ictal state with delayed return to baseline;
tongue lacerations with tonic clonic movement

SLE induced seizures;

Manifestationn; fever, fatigue, weight loss
Symmetric migratory arthritis, skin will cause butterfly rash, photosensitivity, serositis, pleurisy,
pericarditis, peritonitis, neurologic---cognitive dysfunction and seizures

Laboratory findings; hemolytic anemia, thrombocytopaenia, leukopenia; hypercomplimentemia

(C3/C4), ANA (sensitive) and anti-DsDNA, and elevated creatinninie.

SLE: this is a multisystem disease; that will show CNS manifestations; they may be normal or
have mild inflammation

CO Poisoninng;
Epidemiology; smoke inhalation; defective heat systems, gas motors operating in poorly
ventilated areas
Manifestations; mild, moderate, headache, confusion---severe, seizures, sycope and coma,
myocardial ischemia, arrhythmias
Diagnosis; ABGs and carboxyhemoglobin

Note that there will be cerebral hypoxia; this includes headache, nausea, dizziness, and
confusion along with lateral tongue biting;
Coximetry of ABGs will show elevated carboxyhemoglobin levels

In sum, CO poisoning, this will be due to faulty indoor heating systems during winter, both 02
delivery and usage are disrupted; this will lead to hypoxia (headache, confusion, seizure, coma
and death)

Concussion; this will be a transient neurologic event; (disorientation, amnesia) from mild TBI
- This will cause patient to undergo thorough neurologic exam with CT scan; this is for
those considered high risk
- Management; gradual return to play protocol; increased activity in increments

Concussionn; transient neurologic disturbance ( disorientation and amnesia, mild TBI)

headache, slurred speech and incoordination, rest > 24 hours before returning to contact sports

Concussion; this will develop disorientatin post head injury/trauma

Pathogenesis; there will be transient disturbance of normal neuronal function; th typical
symptoms are headache, disorientation, amnesia; also vomiting and LOC;
- I sum, connfussion, mild TBI; transient impairment of normal neuronal function;
headache, disturbance and amnesia; with abnormalities in speech attention and
emotions

Guillan Barre Syndrome;

Pathophysiology; this is an immune mediated demylenating polyneuropathy, preceded
gastrointestinal campylobacter jejuni
Clinical; paresthesia, neuropathic pain, symmetric ascending weakness
- There will be normal MRI----or enhancement of anterior nerve roots
- Management; monitoring autonomic or resp function
GBS; there will be peripheral nerve function with motor polyneuropathy, sensory symptoms—
MRI will affect peripheral nerves

GBS: there will be rapidly progressive ascending motor weakness; there will be immune
mediated demylenation;

Hemorrhagic Stroke;
Overview; the patient presents with an acute episode of right sided weakness and slurred
speech; , hemispheric lesion (Particularly the motor Cortex, and Broca’s area); this will have
neurologic symptoms; (hemiplegia, hemiparesis, and hemisensory disturbances)
- This will have acute onset of unilateral oneisded weakess and slurred speech (ICH); this
will occur over a few minutes and will cause increased ICP; with vomiting, headache
bradycardia (Cushing triad), HTN, irregular breathing and decreased alertness

Incorrect; HHS: this will present in type II DM, with AMS: this will not start until blood glucose >
600, mostl above 1000---
Carotid Artery atherosclerosis; cerebral hemispheric ischemia

Educational goal; HTN encephalopathy; BG, thalamus; can progress to elevated ICP

Hemorrhagi stroke in AD:

There will be cerebral amyloid angiopathy; leads to lobar intracranial hemorrhage
CAA; there will be abnormal b-pleated shehets, can accumulate the blood vessels and lead to
spontaneous ICH;
Managementl reverse anticoagulation, normalize ICP
Educational goal; cerebral amyloid angopathy; occurs due to beta amyloid deposition in small
vessel walls; there will be increased vascular frailty;

Stroke Management;
Assessment of the ABCs (Airway breathing circulation): noncontrst head CT; ischemic stroke BP
control,
Hemorhagic stroke 140-160, reverse anticoagulation maintain ICP
BP Control (IV nnicardiphie and labetolol) 140-150
Anticoagulationn reversal; warfarin and protamine)

Hemorrhagic Stroke In Children :

Risk factors; vascular malformations; AVM, aneurysm;
Hemotologic Malignancies; Hemophilia, and SCD
Clinical features; headache, vomiting, seizures focal neurological deficits, AMS
Imaging: Head CT, intraparynchmla;;
Mannagement; supportive care----AVMS; isolated congenital disorders associated with
mucocutaneous formations (AVMs) and raised risk of hemorrhagic stroke
- There will be headache, vomiting; increased ICP

Alcohol Withdrawal; there is acute confusion, restlessness, visual/tactile hallucinnationnns

- It will enhance GABA and reduce NMDA; (6-24 hours post alcohol cessation), with
alcohol hallucinations; this will prominently feature insects or animals and DT (will show
extreme autonomic instability with fever and diaphoresis)
- Management; benzodiazapines)
Generalized Status epilepticus; this is defined as a seizure >5 minutes, there is no complete
regaining of consciousness; this will occur with tumour/stroke; innfeciton; hypoglycemia;
 - This will be first managed with ABCs; concomittmently IV benzodiazpinnes should be
donne to prevent seizure recurrannce;

In sum, generalized convulsive status; ?5 minutes; benzodiazepine/diazepam, should be

administered to prevent recurrence; with fosphenytoinn, phenytoin, levitaractam and valproic
acid

Phenytoin; This is a commonly used long acting anti-eplieptic medication inhibition voltage
gated sodium channels; will present with signs of cerellar dysfunction, horizontal nystagmus;
and AMS

Sttus Epilepticus; this will be in the setting disorder rand noncompliance; there will be
associated with epilepsy-----however, due to hyperceitability; there Is an increased risk for
necrosis
- Educational goal; recent studies have shown that a brain that has seized for > 5 minutes;
increased risk for excitatory cytotoxicity; the highlight is cortical laminar necrosis

ICP Reduction
Decrease parynchymal volume; osmotic therapy (hypertonic saline, mannitol, to extract water)
Decreased blood volume
- There will be increased risk for ICP; there cerebral blood flow, the CSF and the
intraparynchmal volume; are the big determinants
- PaCO2 this is the greater regulator than p02
ICP; this cann be lowered and reduced metabolic demand,
Educational goal; short term hyperventilation; lowers ICP causes cerebral washout of CO2;
leading to vasoconstriction and reduced cerebral blood flow

Carbon Monoxide Poisoning;

Epidemiology; there will be caused by smoke inhalation; defective heating systems and gas
motors in poorly ventilated areas
Mild/moderate; headache, confusion, malaise, dizziness, nausea, severe, syncope and coma
Diagnosis; ABG; carboxyhemoglobin, ECG and cardiac enzymes
- Management 100% high flow O2 and intubation
- There will be cerebral hypoperfusion, dizziness and confusion, can have MI, seizures
(shown with tounge biting) coma and death
- Diagnosis; co-oximetry of ABGs
- Carbon monoxide; this is due to faulty indoor heating systems; there will be cerebral
hypoxia, headache, confusion, coma and death with elevated carboxyhemobloin levels

Pediatrics
Vitamin K; this is a cofactor in 2, 7,9 10; there will be poor placental transfer, absent gut glora,
poor vitamin K use, intramuscular K; there will be exclusively breast fed; there will have
hyperdense fluid collection in the posterior ventricles;---vomiting, irritability, bradycardia with
bulging fontanelle, rapidly enlarging head circumference with downward gaze

Newborns who do not obtain IM vitamin K are at risk of bleeding, ICH, there will be onstructive
hydrocephalus and signs of increased ICP; irritability, vomiting, bradycardia and HTN

Vitamin Defieicny; this will cause intracranial hemorrhage and obstructive hydrocephalus; this
is a key factor in 2,7, 9 and 10; it is normally administered at birth to prevent bleeding
- It can present at 2 weeks and 6 months to prevent bleeding; this will lead to obstructive
hydrocephalus; it will show irritability, vomtig, brady HTNN
Patients who do not obtain IM vitamin are at risk for vitamin K deficiency bleeding; easy
bruising bleeding

Niemann Pick Syndrome; type A; the type A is the most severe but B and C are milder;
This is a progressive, AR disease; loss of motor milestones at age 2-6 moths with
hepatosplenomegaly; cherry red macula

Tay Sachs; this is an AR disease; but there will be a hexose b-amadase pathway;
Krabbe; this is galactocerebrocidase; developmental regression areflexia
Gaucher; glucocerebosidase; anemia, thrombocytopaenia and hepatosplenomegaly

Rett Syndrome
Key Features this is a rare neurodevelopmenta disorder; 6-18 ,months, loss of speech,
purposeful eye movement gait abnormalities
Abnormal findings; head growth deceleration, seizures, breathing abnormalities, autistic
features
- Etiology; MECP2
Overview this is an X linked genetic disorder; this will have neurodevelopmental regression post
period of normal development; sterotyped movements and gait disturbance
DNA analysis; identify pathogenic mutants;

In sum, rett syndrome; girls, neurodevelopmental regression, loss of speech and purposeful
hand movement; MECP2 confirms diagnosis

Fragile X Syndrome (Trinucleotide CGG repeats; gene methylation silences FMR production
Gene methylation silences FMR production
Neuropsychiatric issues; developmental delay, intellectual disability, ADHD, ASD< self injurious
behaviour and anxiety
Examination findings; long face with prominent forehead, large protruding ears, macroorchism,
macrocephaly
Diagnosis; FMR1 DNA analysis

Other neurodevelopmental disorders

Rett Sydnrome; progressive brain detoriation that leads to microcephaly and developmental
regression; this in MECP2; in women, fatal in boys

Breath Holding Spells;

This will be a common cause for sycope (BHS), these are cyaotic and pallor; cyanotic will lead to
vigorous crying, breath holding and LOC
Pallid; this will be after minor trauma, the child will become pale and diaphoretic, the patient
will be sleepy and confused
BHS clinical with no further testig

Pallid breath holding spells; caused by fear or pain from minor trauma; characterized by pallor
followed by sleepiness and confusion, clinical diagnosis no testing needed

Myotonic Dystrophy; this is most common in the adolescent and adult onset AD (CTG
expansion in the dystrophia, myotonica protein kinase; there is CTG repeats; which will have
dysphagia, other manifestations include atrophy and infertility

DDx; Duchenne and Becker; XLR; this is caused by sporadic de novo mutations; with progressive
and proximal weakness
- There will be AD; presents in adolescence,and early adulthood with myotonia; muscle
relaxation, progressive weakness (facial and hand muscles), dysphagia, and cardiac
conduction abnormalities, atrophy and infertility can occur

Surgery
TBI management
1. Maintain MAP isotonic fluids and pressors
2. Reduce ICP; head elevation, sedation, osmotic therapy
3. Desmopressive intervention---CSF remova and craniectomy

Prevent ICH; can use TXA; reversal of anticoagulation

Other measures; prevent seizures; leveteracitam, phenytoin, control blood glucose Insulin 140-
180 and maintainance of normothermia (antipyretics and surface cooling)
TXA; antifibrinoltuc; this will be beneficial for mild TBI or severe TBI

In sum, acute traumatic coagulability; will have hypercoagulability and hyperfibrinolysis; with
antifibrinolytic therapy to enhance outcomes with moderate bleeding post hours after injury

Cervical Radiculopathy; there wil be a diminished biceps reflex suggesting peripheral NS

involvement (there will be median, ulnar, dermatomal distribution (cervical radiculopathy_
- This is due to spinal nerve root compression; nec and shoulder pain with lateral flexion;
management shoulder abduction relief test ( diagnostic and therapeutic)
Parosyxmal SNS Hyperactivity;
This will be sudden onset of SNS activity; this will be linked to TBI; there will be damage to
cortical areas with severe TBI; there will inhibit lower SNS pathways; triggered by exertnal
stimuli
Triggers; avoid GABA agonists, opiods, and prevet episodes

Traumatic Brain Injury;

Maintain MAP: isotonic fluids, vasopressor therapy, reduced ICP: head elevation, sedation,
osmotic therapy (CSF removal and craniectomy)
- Prevent ICH: antifibrinolytic therapy (TXA2), this will be within the first 3 hours, reversal
of pre-existing anticoagulation
- - there will be hypercoagulability; and hyperfibrinolysis

Educational goal; acute traumatic coagulopathy, there is a state of hypercoagulability and

hyperfibrinolysis; TXA can improve outcomes for patients with moderate TBI if administered
first three hours post injury

Spinal Cord iNjury; there will becaused by anterior subluxation of C6, C6; this will be caused by
C6l this will be associated with radiculopathy
- C5/C6; this will be associated with wrist extension and numbness of the forearm ad
wrist
Educational goal; Cervical facet dislocation, forced flexion of the cervica spinne, fallig on a
flexed nnecl there will be associated with C5/C6; imaginng dermatomes anterior subluxation

Cervical Radiculopathy;
C5; this will manifest with bicep involvement in the lateral upper arm; this will also have issued
with shoulder abduction and elbow flexion
C6; this willcause prblems with elbow flexion
C7; issues with elbow extension, wrist flexion and finger extension
- Compression of nerve root; due to disc herniation; there will mostly be gradual
resolution, so avoid provocative maneuvers

Cervical Radiculopathy
There will be back and shoulder pain; there is loss of shoulder abduction strength; reduced
sensation---in the left lateral forearm (C5-6); this will form a cervical radiculopathy; this will
cause herniation revealing underlying cervical spondylosis
- Evaluation begins with MRI of the cervical spine
Educational goal; cervical radiculopathy common in older individuals, post physical activity and
trauma placing strsss on the neck

Anterior Cord Syndrome

- There will e a devastating complication; 5-15% odf TAA, ti can disrupt SC flow, there will
be SC hypoperfusion; leading to segmental artery disruption;
- Presentation; bilateral paralysis from damage to the LC and anterior horn cells
 - Loss of pain temp from spinothalamic tract
PC; this will be intact as vibration is normal

Thoracic Aortic annerysm; this will cause SC ischemia; especially at the annnteior cord; loss of
pain, temp crude touch sensation and urinary retention

Carotid Artery Dissection

Pathogenesis; Penetrating trauma, and fall with object in mouth----toothbrush and pencil, neck
manipulation
Presentation; gradual onset hemiplegia, aphasia, neck pain, thunderclap headache
- Diagnosis; CT/MR angiogram
Carotid artery complications; penetrating oropharyngeal trauma (fall down a tree); there will be
raised risk of dissection; hemiparesis, facial droop and aphasia----

Differential; todd paralysis; this is transient hemiplegia post seizure

Educational goal; oropharyngeal injuries; this will result in ICA dissection or thrombus
formation; there will be facial droop, aphasia

Spinal Epidural Hematoma; SHE; this will be a potential complication of neuroaxia; anesthesia;
LP and spinal surgery; this will be common for those taking antithrombin medication----
management urgent MRI of the spine

In sum, spinal epidural hematoma; potential complication of neuraxial anesthesia (spinal block,
LP, spinal surgery; more common in older adults taking antithrombin medication

Epidural Hematoma;
Pathogenesis; this will be trauma to the sphenoid bone with tearing of the middle meningeal
artery
- There will be a brief loss of consciousness; with a lucid interval; elevated ICP and unca
herniation; CT scan of the head; will be biconves, will not cross the suture lines
- Treatment; surgical evacuation
EDH: this is accumulaton of the blood causses increased ICP

Traumatic Injury to the left eye;

There will be inflammation, conjunctival erythema; this is most consistent with sympathetic
opthalmia; an AI disease where the eye is sensiztied to previously unsensitized antigens; there
will be an inflammatory response; management eye is enucleated to halt blindness
Neurocutaneous Syndromes;
NFII: this is localized on chromosome 22 and it encodes Merlin (there is variable expressivity at
ages 20-30)
Clinical manifestation; vesticular schwannoma, intracranial meningioma,, spinal tumours,
cataracts and cutaneous plaques or tumours
Mangement; surveillance, audiogram and MRI

NFII: will have > 95% develop sensorneural hearing loss, it is an AD defect (merlin)

NFI: this is an AD neurocutaneous syndrome with café au lait spots and cutaneous
manifestations appearing in infancy; there will be done with increasing age, axillary/inguinal
frecles and neurofibromas
- Positive optic glioma, this will also have headaches and decreased visual acuity with
morning headache,
- Managemnet; 1. MRI of the brain and orbits

NF2; this will have acoustic neuromas bilaterally; this can lead to sensorineural hearing loss;
ESR; this is an acute phase reactant in the setting of inflammation
LP; this will rule out meningoencephalitis

Educatioal goal; this will have optic pathway gliomas, decreased visual acuity and MRI of the
brain and orbits evaluate for an intracranial mass.

NF1; there will be optic glioma, lisch nodules, café au lait macules, scoliosis and neurofibromas
- This is an AD disease with café au lait spots; there will be increased age

NF1;
There will be seizure activity; there will be skin findings---with neurofibromatosis; this will be
caused by NF1; this will be at increased risk of neurological disorders (Cognitive deficits,
learning defects, and intracranial neoplasm)

NFI; this is an autosomal dominant neurocutaneous disorder associated with freckling, seizures,
learning disabilities optic pathway gliomas

Tuberous Sclerosis;
Pathophysiology; (mutation, inherited or De novo), autosomal dominant
Clinicial features; ash leaf spots, angiofibromas, shagreen patches
- CNS lesions, epilepsy; intellectual disability, autism and behavioural disorders
- CV; will cause rhabdomyomas and renal we see angiomyilipoma
Tumour screening; regular skin.eye exams;s erial MRI and baseline ECG
- This will cause ID, developmental delay; cortical glioneuronal hamartoma,
subependymal nodules; with hypopigmented macules and shagreen patches
TSC; this will show refractory epilepsy, developmental delay ID, skin findings (ash leaf spots),
subependymal nodules

Sturge Weber Disease

Mutation in GNAQ
Will have port wine stain (CN V1, V2 distribution, leptomeningeal capillary venous
malformation, ID, visual field defects, glaucoma,
Diagnosis; MRI of the brain with contrast
Management; laser therapy, antiepileptic drugs; this will be nevus flammeus; this is a port wine
stain of the trigeminal nerve; associated with ID; this will cause developmenta; delays beginning
in early childhood; MRI; this will detect intracranial vascular malformation; it is diagnostic

Sturge weber; neurocutaneous disorder with a capillary malformation, port wine distribution,
leptomeningeal capillary venous malformation manifesting in the brain and eye
Radiculopathy;
C5; this will be innervated by the biceps; there is shoulder abduction and elbow flexio

Interventions to reduce intracranial pressure

1. Decrease brain paranchyma volume; osmotic therapy
2. Decreased brain parenchymal volume; there is head elevation to increase venous
outflow;
3. CSF removal
4. Decompressive craniectomy

There will be elevated ICP; HTN, bradycardia and irregular respiraitons and diffuse cerebral
edema on imaging; provide hypertonic saline to reduce risk of cerebral herniation

Osmotic therapy; hypertonic saline, mannitol, part of initial treatment for elevated ICP
Educational goal; osmotic therapy (hypertonic saline/mannitol; this is part of the initial
treatment for ICP it will create osmolar gradient to draw out water from the edematous brain
tissue and reduce ICP

Infectious Diseases;
Brain abscess; there is risk for mastoiditis; dental infection, cyanotic heart disease---
- Cyanotic congenital heart disease (TOF), this will raise the risk for brain abscess; this will
cause a right to left shunt----
- Headache; will have vomiting particularly in the morning; there is a fever and focal
neurological changes

Hypocalcemia; this is a common featue of Digeorge; however, it will not explain the fever
Educational objective; there will be headache, fever, focal neurologic deficits and seizures;
there is a risk for brain abscess due to bacterial spread

Rabies;
Pathogenesis; transmission by the rabies virus by a bite from an infected mammal
Reservoir; United states, bats, raccoons, skunks, foxes,
Encephalopathic; hydrophobia, aerophbia, spasticity, agitation AMS,
Post exposure prophylaxis; Rabies immunoglobulin and vaccine series
Coma; resp failure and death in few weeks
- There will be bats and racoons that will cause symptoms 1-3 months with numbness inn
the wound there will be encepahlopathys symptoms such as sspasms and dysautonomia
Rabies; this is a fatal neurotropic viral disease with exposure to saliva from an infectious agent ,
period 1-3 months with dysautonomia; hydrophibia, coma and death

CSF Fluid Analysis;

Bacterial Meningitis; Neutrophils; there will be progressive headache, vomiting, low grade fever
and nuhal rigidity; *pathogenesis; strep pneumo;---suggests cryptococcal meningitis;
- There will be risk with immunosuppressive medication
- Subacute manifestaitons
Diagnosis; this will require encapsulated yeast

Educationnal goal;s AIDS; solid end organ transplantation, raised risk for cryptococus; this will
have lymphocytosis with mildly elevated WBC and low glucose

HSV Encephalitis;
Clinical features; fever, headache, seizure, AMS (Confusion agitation)
Focal neurologic findings (hemiparesis, craial nerve palsies)
Diagnostic findings; elevated WBC, RBC, protein and normal glucose
Treatment; IV acyclovir
- There will be seizures/fever, AMS and focal neurologic findings----HSV there will be
changes in the trigeminal ganglion with hemorrhage and edema
Reye syndrome; this will have liver dysfunction, will preent with generalized seizures post viral
illess

AMS; fever, headaches, seizure, temporl lobe abnormalities and edema are highly suggestive of
HSV encephalitis

PNES
Clinical features; observed during wakefulness with a long fluctuating course, asynchronous
thrashing, pelvic thursting, no LOC
Comorbidities; psychiatric condisions; depression, anxiety, PE/sexual abuse,
Diagnosis; Video EEG
Treatment; CBT

PNES; pseudooseizures; this will occur in the presense of witnesses; there is eye closure and
fluttering during the spell; side to side head shaking, asynchronous limb movement and lack of
post ictal period; manage with video EEG

PNES; this is similar to epilepsy; not associated with increased synchronous features; use video
EEG to capture and characterize a spell prior to treatment.

PNES: there will be seizure behaviour associated with forceful eye closure, absence of self
injury, incontinence and post ictal confusion; this is a subet of conversion disorder---occurs in
front of witnesses; there will be modeling behaviour post friend or relative with epilepsy
- There will be not associated with abnormal cortical activity; Video EEG: this is gold
standard as it will demonstrate lack of associated epileptiform activity
PNES: this is a conversionnn disorder; this will misdiagnosed as seizure , forceful eye closure,
side to side body moements and lack of post-ictal confusion

Tabes Dorsalis; This will occur over years; decades following initial infection; there Is increased
incidence and more rapid progression
Pathogenesis; T. Pallidum, this will directly damage the dorsal column
Clinical findings; there is sensory ataxia, lancinating pains, neurogenic urinary incontinence,
associated with Argyll Robertson pupils
Treatment; 10-14 days of IV penicillin G

Tabes dorsalis; this is a neurodegenerative disease---there is impaired vibration;

sensation/proprioception, insability with Romburg maneuver;
- Management will be with IV aqueous crystallin penicillin

DDx
Wernike Korsakoff; there will be ataxia, encephalopathy and opthalmoplegia; with nystagmus
and lateral rectus/gaze palsy.

B12; there will be subacute combined degeneration; there is absent vibration sense; positive
ROmburg sign;

In sum, late neurosyphilis manifests years post untreated t. pallidum,with generalized paresis
(sensory ataxia, lancinating pain)

Botulism;
This is a case of infant botulism, highest incidence is in Calfornia with the highest concetration
of salt botulism spores from the environment; note that raw honey is another risk factor; we
suspect this diagnosis in bulbar palsy; there is descending flaccid paralysis (hypotonia,
constipation and drooling are other risk factors

- DDX; GBS; this will be a demylenating polyradiculoneuropathy; it will cause paralysis inn
the lower extremities
- MG; this will have lack of autonomic symptoms such as constipation, drooling anndn
generalized hypotonia
- Werdnig Hoffman Disease; generalized symmetry and hyporeflexia; this does nnot affect
the pupils
- Educational goal; this is going to colonize the gut and lead to life threatening flaccid
paralysis; characterize with bulbar palsy, constipation and hypotonia even if the
individual has not been fed honey

Sleep Disorders;
Narcolepsy; there will be recurrent lapses into sleep/naps > 3 times a week for 3 months; there
is cataplexy; brief loss of muscle tone precipitated by strong emotion (such as excitement) );
associated features hypnagogic or hypnopompic hallucinations and sleep paralysis
- There is cataplexy; this is transient loss of muscle tone in response to intense emotion,
this is suggestive of REM sleep phenomena and seel paralysis s
- There will be low levels of orexin; hypocretin 1

Narcoplesy; excessive daytime sleepiness, cataplexy and REM sleep related phenomena with
hypnagogic and hypnopompic hallucinations

Narcolepsy; there will be recurrent lapses into sleep/naps > 3 times/week for 3 monhs, there is
also associated cataplexy, brief loss of muscle tone; low CSF of hypocretin 1
- There will be association with low levels of CSF, orexinA/ hypocretin-1; there will be
multiple sleep latency and sleep-onset REM
Narcolepsy; there will be excessive daytime sleepiness, cataplexy and REM sleep related
phenomena; there is also hallucinations and sleep paralysis

Psychiatry; Serotonin syndrome;

Causes; SSRI/SNRI, TCA, tramadol, drug interactions with serotonergic medication &MAOI and
linezolid
Intentional OD of serotonergic medication
MDMA abuse
- There is mental status change, such as anxiety, agitation and delirium; NMJ
hyperactivity; tremor, myoclonus and hyperreflexia
- Management; discontinuation of all serotonergic meds; benzodiazepine

- Sertraline; this is an SSRI; tramadol, this is an analgesic medication with serotonergic

activity
In sum, there is mental status change, autonomic dysregulation, NMJ hyperactivity (tremor,
bowel sounds)

Serotonin Syndrome; Serotonergic medications; combination (SSRI/SNRI), TCA, tramadol

Drug interactions; this will be associated with serotnergic medications, MAOI, and linelzolid,
intentional overdose of serotonergic medications
Clinical features; MS changes (anxiety, agitation, delirium, ANS dysfunction (diaphoresis, HTN,
tachycardia), NMS hyperactivity
- There will be increased anxiety, restlessness, and PE findings (Jitteriness, diaphoresis,
HTN and increased muscle tone; sertraline is an SSRI uptake inhibitor for generalized
seizure with serotonergic meds

Educational goal; serotonin syndrome; this is characterized by MS changes, ANS dysregylation

and an unintentional result with combined use of serotonergic agents (SSRI)

Acute Dystonia; this will be ann abrupt onset; reaction; extrapyramidal symptoms will be able
to cause an oculogyric crisis; there will be forced upward gaze deviation; other findings are
torticollis; blepharospasm and trismus;
- This will be managed by benztropine;

DDx; NMS; use dantrolene; path, high potency antipsychotics; hyperthermia, tachycardia HTN
Fosphenytoin; for Status

In sum, dystonia; involutary muscle contaction; hand and neck, ocylogyric crisis; haldol and
fluphenazine

Tardive dyskinesia; this is an involuntary movement disorder with DA blocking agents

- Characteristic movements include orofacial dyskinesia----the pathophsyilogy of this
disease is D2 upregulation; the blo
MDD;
Normal aging; delayed in fluid intelligence; cannot process new infroamtion quickly
Mild neurocognitive disorder; decline inn ADLS with compensation
Dementia; > 1 decline in cognition, irreversible
MDD: reversal (depression, mood innteest and energy)
- There will be reversible dementia; complete resolution of the cognitiveimpairment;

Educational goa;; this will have severe cognitive impairment mistaken for dementia, however it
is treated by treating underlying dementia

Catatonia;
Clinical features; there is immobility; or excessive purposeless, mutism, stupor, negativism,
waxy flexibility; echolalia; echopraxia, benzodiazepine, ECT; there will be immobility, mutism,
nnegativism; management (benzodiazepines)

Educational goal; immobility,mutism, negativism, echophenomenna; settting of BPD, MDD<

management; benzodiazapines

REM Sleep Behaviour Disorder;

There will be complex motor behaviour that occurs during REM Sleep

Social Sciences;
Aggressive patient in the ED
History of violent behaviour and antisocial personality with psychiatric illness such as psychosis,
delirium, acute intoxication, withdrawal along with prolonged wait times

Warning signs; angry and irritable demeanor; loud/aggressive speech, cursing and verbal abuse;
tense posturing and clenched fists/pacing

Maintain a distance of two arm lengths door opened with clinician close to exit; with a
nonconfrontational voice, provide for basic needs, listen attentively and clarify patient wishes,
and set clear expectations

Child Abuse;
Subdural hematoma;
Risk factors; unstable family situation, there will be vague history and injury inconsistent with
the developmental stage
Clinical features; bruises, fractures at various stages of healing; femur fracture, posterior rib
fracture
Management; skeletal survey, CT scan and fundoscopy

Abusive head trauma (shaken baby syndrome); the infant is particularly susceptible---will show
shearing of bridging veins and coup contrecoup injury

Mechanism of injury is inconsistent; CT scan noncontrasr

Agitation; begin with decelerating the situation and using restraints as a last resort, the patient
is currently agitated and uncooperative and having difficulty
- Respect for personal space, calm voice, nonthreatening demeanor and setting limits on
harming onsself and staff is not permissible
Managing Difficult Situations
The patient remains symptomtic despite multiple mediation trials; this is frustrating and can
leave doctor annnngry; the best approach is to empathsize with limited expectations

Emergency Medicine
Common exposure; Pesticide farmer/field worker, pediatric ingestion and suicide attempt;
nerve agent; multiple patients presenting with similar symptoms

Manifestations; DUMBELLS (Diarrhea, diaphoresis, miosis, bronchospasm, bronchorrhea,

bradycardia, emesis, lacrimation, salivation; nicotinic *Muscle weakness, paralysis, ad
fasiculations

Cholinergic toxicity; this is likely due to organophosphate pesticide exposure (ABCs)

/decontamination; pralodixme will cause transient ach inhibition

Organophosphates inhibit achesterase; this will lead to the DUMBELLS; cholinergic

hyperstimulation, management includes atropine, this is a competitive inhibitor of achesterase
followed by pralidoxime

Ocular Trauma;
Optic nerve injury; this will have indirect shearing forces; direct---penetrating eye trauma
Clinical features; this wlll manifest with acute vision loss, decreased colour vision and afferent
pupillary defect
Diagnosis; CT scan of the orbit
- Relative afferent pupillary defect; will common;y be indirect----this will be confirmed by
CT

Educational goal; optic nerve injuries; may occur post head trauma; there will be a decrease in
visual acuity and a RAPD in the injured eye

Concussion;
Mild head trauma; occurs in children and adolescents and does not lead to long erm
complications,---high risk features; AMS, LOC, and severe mechanism of injury high impact hit,
- High risk features; AMS, LOC severe mechanism of injury
Head CT without contrast; is preferred imaging; modality----this is indicated with AMS, LOC,
severe headache, no signs of basilar fracture

Concussion; this is caused from recent motor vehicle collision; there will be due to rapid
rotational acceleration results in neurologic disturbance with no structural injury; there will be
headache; light and noise sensitivity are common and are coupled with emotional changes
Concussion; caused by rapid rotational acceleration during head trauma;

Neurologic Pain Disorders;

Trigeminal Neuralgia; this will have recurrent and sudden onset severe symptoms affectingng
V3; mandibular branches of the trigeminal nerve; this is stimulated by touch, wind and chewing
MS; this will affect trigeminal nerve bilaterally; this will have severe paroxysms of pain

HZ; this is caused by viral reactivation leading to neuritis; when the V1 brnach is involved it wil
lead to HZ opthalmicus
Cavervnous sinus thrombosis; will affect CN 3,4, 6 and V1,2 (ophthalmic and maxillary
brannnches)

Distal symmetrical Polyneuropathy

There is bilateral numbness/pain with loss of sensation; this will show distal symmetrical
polyneuropathy is long standing HIV and low CD4 count; this will have long standing HIV
Management antiretroviral therapy

HIV neuropathy; begins with numbness, tingling and pain; there will be management with
antiretrovial therapy; gabapentin is first line

Distal Symmetric polyneirpathy

Triggers; DM< long stnding HIV< uremia, medication, chemotherapy, toxicity
Pathophysiology; damage to the sensory peripheral nerves , remia, medications, chemotherapy
- Manifestation begins in the toe/feet and progresses proximally over time
- Treatment; manage underlying cause;
- Polyneuropathy; this is caused by DM, HIV infection, annnd acute polyneuropathy---this
can cause metronidazole,cessation of the offending medication is the first step
Progressive sensory loss, distal symmetric stocking glove distribution; axonal polyneuropathy,

Movement Disorders
Blepharospasm; this is bilateral and symmetric; it is associated with spasm of the lower face,
jaw and tounge; with bright lights triggering muscle contraction leading to a sensory tick; there
will be botulinum toxin needed for more significant symptoms

- Blepharosm; recurrent forceful contraction of the eyelid; caused by touching or brushing

skin; for more severe cases nneed botulinum toxin

Parkinsons Disease; Neurodegenerative Disease; associated with a-synucelin in the Snc; the
three cardinal signs of PD’ corroborated by PE; will be used to confirm diagnosis

Findings for PD ; tremor 4-6 hz tremor with a pill rolling quality, it will manifest in one hand and
will migrate to another
Rigidity; there is increased resisitance to passive movement
Bradykinesia; there will be difficulty iniitatinng movement, narrow based shuffling gait,
micrographia, hypomimia, and hyphonia, postural instability; flexed axial position,postural
instability----loss of balance during turning and stopping,
3 cardinal signs of PD; rest, tremor, rigidity, and bradykinesia;
Orthostatic Hypotension; Parkinsons disease;
NOH (Neurogenic orthostatic hypotension this is common in PD (Lewy Body dementia, MSA)
this will manifest with lightheadedness; syncope on standing;in the normal state from standing
from seated to supine; there will be triggering of vasoconconstriction; this will mobilize pooled
venous blood;
- NOH: there will be a drop in SBP > 20 and DBP > 10

DA; this can treat the motor symptoms of PD; however it will cause vasodilation
Educational goal; ANNS Dysfunction with PD: leads to neurogenic orthostatic hypotension with
lightheadedness, there will be a > 20 mmhg in SBP and absence of expected increase in HR

Seizure vs. Syncope;

Eileptic seizure, this will be caused by hypersyncronization of electrical brain networks with
involuntary movement and associated LOC; there will be TIA< migraine, LOC, panic attack
Post recovery episodes; variable minutes, to hours, to days; with residual confusion
Eplletic seizure; ddx; there will be high specicity for tongue biting, especially lateral tounnge
biting

Educational goal; eepileptic seizure; will be difficult to differentiate from syncope, tongue biting
is common (lateral tongue specific for epileptsy

CIPD:
Pathophsyiology; immune mediated demylenaton of the peripheral nerves and roots, it is
nonlenngth dependant
Clinical progression > 8 weks, motor > sensory, proximal and distal weakness, hyporeflexia,
atrophy
CSF: elevated proteins, normal WBC, decreased conduction velocity, segmental demylenation
Treatment; glucocorticoids, IVIG, plasmapheresis
CIPD; this is an acquired immune mediated disorder; demylenation of peripheral roots and
nerves; there will not be length dependant; ahnd weakness >8 weeks; LMN signs
*hyporeflexia), evidence of demylenation; decreased peripheral nerve conduction velocity

Vasovagal Syncope;
Triggers; pain, anxiety, emotional stress, head, prolonged standing
Situational; cough, micturition, defecation, eating and hair combinng
Diagnosis; mainly based on clinical history of event; upright tilt table test
Treatment; reassurance, and counterpressure techniques for recurrent episodes;
- There will be prodromal symptoms; dizziness, nausea, diaphoresis, abdominal pain, and
generalized sense of warmth
- Recurrent syncope; there will be supine position with leg raising with physical
counterpressure maneuvers;
 - Educational goal; general treatment with vasovagal syncope, reassurance, education---
counterpressure to abort or delay the episode of syncope
Ambulatory Medicine
GI; diarrhea, steatorrhea, weight loss, abdominal pain, flatulence, bloating---later
manifestations, UC, enteropathy
Mucocutaneous; dermatitis herpatiformis, atrophic gastritis,
Endocrine; vitamin D deficiency, secondary hyperparathyroidism
Bone disorders; osteomalacia, osteoporosis
Rickets; Hematologic; IDA
Neuropsychiatric, peripheral neuropathy, depression/anxiety

Length dependant axonal polyneuropathy; IDA, atrophic glossitis;

- Educational goal; celiac disease can present diverse array of symptoms related to
malabsorption; (autoimmune inflammation) atrophic glossitis