NEUROLOGY

TOPICS

NEUROSURGERY NEUROMEDICINE

1. SUBARACHNOID HEMORRHAGE 1. HEADACHE

2. HEAD INJURY 2. STROKE

3. LOW BACK PAIN 3. MULTIPLE SCLEROSIS

4. CONGENITAL ANOMALIES 4. MOVEMENT DISORDER

5. BRAIN TUMOR 5. SEIZURE

6. PERIPHERAL NERVE DISEASE

Neurosurgery
Subarachnoid hemorrhage
-blood within CSF

-causes: Clinical features

1. Trauma 1. Sudden severe headache
2. Rupture berry aneurysm 2. LOC
= ant circulation: Acom> Pcom > MCA 3. Blurry vision ( optic hemorrhage/ optic
= post circulation: basilar tip aneurysm nerve swelling)
3. AVM, vasculitis,tumor, carotid dissection, 4. Vomiting (postrema)
htn 5. Neurological deficit
4. Medication
5. Bleeding problem
6. Pre-truncal non aneurysmal SAH

Berry aneurysm
5% incidence Etiology
Age 55-65  HTN
Female:male 3:2  Atherosclerosis
85-90% in ICA  Congenital predisposition( defect arterial wall)
50-60% have 30 day mortality rate  Infection/mycotic aneurysm
60% mortality rate in surviving initial bleed  Traumatic (dissecting aneurysm)
30% occur during sleep  Genetics (PCK, Marfan)
50% have warning sx 1-3 week before SAH

Risk factor Features

 Htn 1. Rupture (95-97%)
 Diurnal BP  Sudden severe headache
 Smoking (thunderclap)
 Alcohol, coffee  Vomiting, kneeling
 Pregnancy, parturition  LOC
 OCP  Blurry vision
 Cocaine abuse  Back pain ( spinal irritation from
blood)
 Meningeal sign
 Sentinel hemorrhage warning
headache
2. Mass effect
 Giant aneurysm
 Compression of 3rd CN
3. Incidental finding
 Rule of 15% Ix
- Die before reaching hosp 1. Non-enhanced CT
- First 24 hr in hosp Why non-enhance?- prevent vasospasm & masking of
- 1-14 days hemorrhage
- 2-8 weeks Other function:
- 2-24 months  Hydrocephalus
25% survive > 2yr  ICH
 Infarction
 Blood in cistern vasospasm
2. LP for CSF
- 3 test tube blood
- Xantochromia
3. MRI helpful after 4-10 days
4. CT/DSA angiogram (4 vessel rule)

Grading
1) hunt and hess

Criteria Value Grade Mortality

Mild Headache, Alert and Oriented, 1 I 30%

Minimal (if any) Nuchal Rigidity

Full Nuchal Rigidity, Moderate-Severe Headache, Alert and Oriented, 2 II 40%

No Neuro Deficit (Besides CN Palsy)

Lethargy or Confusion, Mild Focal Neurological Deficits 3 III 50%

Stuporous, More Severe Focal Deficit 4 IV 80%

Comatose, showing signs of severe neurological impairment (ex: 5 V 90%

posturing)

2) fisher grading system

Modified Fisher Grade Risk of Symptomatic vasospasm

1 no blood detected 6-24%

2 diffuse <1 mm 15-33%

3 localized clot > 1mm 33-35%

4 ICH, IVH 34-40%

Mx

Step 1
 ABC
 GSC, Pupillary reflex
 Admit to ICU
 Intubation
 IV access
 Foley’s cath
 BP keep btw 140-150
 Increased ICP
- Head up 30
- External ventricular drainage
- Osmotic therapy: mannitol, hypertonic saline
- Hyperventilation
- Analgesic/pain sedation: codein phosphate, dexamethasone
- Prophylactic anticonvulsant
 Ca channel blocker- nimodipine
 Statin to prevent vasospasm
 Stool softener, H2 blocker

Surgery
1) clipping
2) coiling (not for unruptured aneurysm)
Step 2
(manage the complication)
Early complication
 Re-bleeding *
 Hydroceph
 Cerebral edema
 Herniation
 Hyponatremia
 Salt-wasting syndrome
 Troponin elevation

Late complication
 Vasospasm ( sx of headache, lethargy, focal deficit, hyponatremia
- Give Ca channel blocker for 21 day  nimodipine, nicardipine
- 3 H protocol ( hypertension, hemodilution, hypervolemia)
- Dexamethasone
- Balloon angioplasty
Vascular malformation
- AVM
- Cavernous angioma
- Venous angioma
- Capillary telangiectasia

AVM
Definition Presentation
-collection of blood vessel where arterial blood  Bleeding
flow direct to veins w/o interposed capillary bed  Seizure
 Mass effect
 Headache, bruit, HF, hydroceph

Ix Treatment
1. CT shows calcification  Excision
2. MRI  Adjunctive therapy
3. Angiogram shows tangle of vessels, (chemo,radio,embolization)
feeders(artery), draining veins  Pre-op B-blocker, dexa, phenytoin

Spletzer & Martin grading

Cavernous angioma
 size of nidus
-sinusoidal vascular channel in brain but lack
o small (<3cm) = 1
intervening neural parenchyma, feeders, draining
o medium (3-6cm) = 2 vein
o large (> 6cm) = 3
-seizure, bleeding, mass , incidental
 eloquence of adjacent brain
o non-eloquent = 0 - CT/MRI show lesion
o eloquent = 1 -treat by excision
 venous drainage
o superficial only = 0
o deep = 1
Head injury
Brain
1. 2% from body Wt. (1400 gm) = actual Wt is 25 gm
2. 18% cardiac blood supply
3. 20% oxygen supply
4. Blood supply 2/3 from carotid artery and 1/3 from vertebral artery

Arteries Venous

CSF
1. 85% produced by choroidal plexus, 15% by surface ventricle+lining of SAS
2. 450 ml/day= 18ml/hr
3. 350ml is absorbed only 150ml circulated ( 75 ml in brain +75ml in spinal cord)
4. Pulsatile on MRI
5. Lack immunity no WBC/ immunoglobulin
6. Function to provide nutrition and for absorption

Cerebral blood flow

1. 55m/100gm per minute
2. It is autoregulated  to meet the brain's metabolic demands.
3. < 18 reversible ischemia, < 8 irreversible ischemia
 Intracranial pressure (ICP)
1. In adult 5-15mmHg Causes:
2. In children <5mmHg  Aneurysm rupture and subarachnoid
3. Brain can tolerate increase ICP without hemorrhage
being drowsy and LOC when  Brain tumor
a) In acute: 25mmHg , if >  Encephalitis
25mmHg abducent and  Head injury
trochlear nerve palsy (sensitive to  Hydrocephalus
ICP)  Hypertensive brain hemorrhage
b) Chronic: 35 mmHg  Intraventricular hemorrhage
 Meningitis
 Subdural hematoma
 Status epilepticus
 Stroke

Sign
Cushing triad HTN, bradycardia, irregular respiration
Symptom
 Behavior changes
 Decreased consciousness
 Headache
 Lethargy
 Neurological symptoms, including weakness, numbness, eye movement problems, and double
vision
 Seizures
 Vomiting
Complication
 Brain herniation
1) supratentorial
- Uncal  compressed brain stem, oculomotor( ipsilateral fixed dilated pupil)
- Central tumor not trauma ( loc, bilateral constricted pupil)
- Cingulate
- Transcranial
2) infratentorial
- Upward cerebellar
- Tonsillar compressed brain stem
1. Traumatic brain injury (TBI)
1ry – irreversible
immediate after injury
2ry- hr/day after injury
-BBB damage
-influx Ca, Na to neuron
3-8 severe
9-12 moderate
13-14 mild
Complication:
 Autonomic dysfunction  HTN, increase T, HR, RR, dilated pupil,
extensor posturing
 Except in: (hypotension)
- Terminal stage of herniation
- Infant with subglial hematoma
- Significant loss blood from scalp
 Cephalohematoma
- Below periosteal layer
- Not crossing midline
- Jaundice, anemia, calcification
 Caput succedaneum
- Diffuse edema
- Not blood
- Cross midline
  Subgaleal hematoma
- Cross midline
- Above periosteal layer
 Degloving
 Compound

Brain concussion
 Commonest type
 Short-lived loss of brain function due to head trauma that resolve spontaneously  because
acceleration and deceleration of brain against the skull glutamate release
 No structural damage seen on imaging
 Temporarily loss of consciousness will occur
 Sx: LOC, headache, slow reaction, dizzy, nausea, difficult with bright an noisy, irritable, change sleep
pattern, amnesia < 24 hr
 No rx
Brain contusion
 Bruise of brain tissue +multiple micro hemorrhage (edema)
 Causes: coup/contue-coup
 Commonly occur in lobes/skull base
 Cx: decline mental function in long term, brain herniation
 Ix: abnormal CT of multiple micro hemorrhage
 Mx: prevent swelling, decompressive craniectomy

1. Brain edema

Definition- excess accumulation of fluid intracellular/ extracellular space of brain

Causes: S&S: Types:

1. Traumatic - N&V 1. Cytotoxic – diffuse edema
2. Non traumatic - Blurry vision BBB intact, steroid C/I
- Ischemic stroke - Coma 2. Vasogenic- around tumor,
- Cancer - Rs arrest BBB deficit, steroid helpful
- Inflammation - Flatted gyri 3. Malignant-head injury,
- Altered cell - Narrowed sulci hyperemia, lost auto
metabolism - Compressed ventricular regulation, mx by
cavities craniotomy
4. Ischemic- blockage, mx by
reducing ICP,
decompressive craniotomy
 3. Skull fracture

-due to blunt force trauma

Types:

Linear Commonest
No intervention
Depressed Inward displacement
May require surgery
*ping pong skull fracture children <2yr , due to soft and cartilaginous nature ,
resolve by pulsation of CSF
Diastatic Widening of suture
Multiple widening in children indicate child abuse
Basilar a) Anterior cranial fossa
- Sx: rhinorrhea, epistaxis, raccoon eye, anosmia, subconjunctival hemorrhage
- CT normal
- Cx: meningitis, pneumochepalus (brain herniation) air appear very dark
b) Middle cranial fossa
- Otorrhea
- Optic nerve injury
- Temporal injury facial palsy and hearing defect
c) Posterior fossa
- Battle sign
Compound A fracture in which broken bone fragments lacerate soft tissue and protrude
through an open wound in the skin.

4. Subdural hemorrhage VS Epidural hemorrhage

Subdural hemorrhage Epidural hemorrhage

 Tearing of bridging veins that cross subdural  Middle meningeal artery tears
space  Sign and symptom
 Crescent shaped on CT - Lucid interval (temporary
 Acute improvement) followed by loc
- High speed injuries - Anisocoria
- Appear hypodense and crescent shaped on CT - Ipsilateral fixed dilated pupil
- Presentation: life threatening, high mortality, - Contralateral hemiparesis
LOC, shift midline - Contralateral exaggerated reflex+
- Rx: craniotomy Babinski sign
 Subactue  Rx: head up, intubation, hyperventilation,
 Chronic mannitol, craniotomy
- Repeated minor bleeding  Biconvex shaped on CT, NO distortion of
- Better prognosis lateral ventrical
- Pt is conscious, midline shift
- Old age, alcoholic, dementia
- Subdural hygroma( csf collection)
- Rx: pure holes, evacuate, craniotomy
 5. Diffuse axonal injuries

- sudden acceleration/ deceleration injuries

- severe persistent LOC
- most common site: white matter (corpus collosum) , brain stem
- MRI

Complication of head injury

Early Late
 Epilepsy cortical contusion, depressed  Post concussion syndrome normal CT
skull fracture, SDH  Leptomeningeal cyst
 Non-convulsive status epilepticus   Carotid cavernous fistula
normal CT, gsc <8  AVM
 Cranial nerve injury  Traumatic aneurysm
 Optic atrophy chronic cause of pupil  Carotid vertebral dissection
dilatation  Endocrine problem
 Optic nerve avulsion insertion of optic  Abscess, meningitis, encephalitis
nerve at lamina  Hydrocephalus  because of meningitis,
 Affected falciform ligament btw optic trauma, IVH
nerve & dura  Degenerative disease Alzheimer,
Parkinson, ALS
 Late epilepsy
 Systemic: arrhythmia, P.edema, infection,
bed sore
 Torticollis  SCM spasm

Management

1. CABC
- C secure by immobilization, neck collar
- A airway
- B intubation, spontaneous breathing, ambu bag
- C circulation
2. VITAL SIGN
- High BP, low HR cushing triad
3. GCS
4. PUPIL REFLEX
5. Neurological examination
6. CBC, blood grouping, cross match, bleeding profile
7. X-ray, US
8. Non enhanced CT ( TBI)
9. MRI DAI (diffuse axonal injury)
Low back pain
- 60-90% incidence
- 90% resolve within 6-12 weeks

Ddx
1. Musculoskeletal pain
2. Lumbar strain
3. Disc bulge,protrusion,extrusion
 radiculopathy
4. Degenerative disc disease
5. Spinal canal stenosis
6. Spondyloarthropathy
(inflammatory joint disease)
 in ankylosing spondylitis
7. Spondylosis (degeneration of intervetebral disc)
8. Spondylolisthesis (one vertebral body is slipped
forward over another)
9. Sacro-iliac dysfunction

Hx:
SOCRATES
 Acute fall, lift, twist
 Subacute inactivity, sitting, driving, flying
 Hx of back pain
 Treatment and response
 Exaggerated factor occupation, recreational, cough, valsalva maneuver

Red flag
TUNAFISH
T- trauma
U- unexplained weight loss, UTI, unrelenting night pain/ at rest
N- neurologic syndrome
A- age 15< or >50
F- fever, failure to improve > 6w of treatments
I- IV drug use, immunosuppressed
S- steroid use
H- hx of cancer, osteoporosis
 Diagnosis and red flag
Cancer Fracture Infection Cauda equine syndrome
 Age> 50  Any age (more in  IVDU SPINE
 Hx of cancer elder)  Steroid user  S-saddle anesthesia
 Significant wt loss  Trauma  Fever  P-pain of lower back
 Unrelenting night pain  Steroid user  Unrelenting night  I-incontinence
 Failure to improve  Osteoporosis pain bowel/bladder
 Failure to improve  N-numbness,weakness
 E-emergency
management
* damage to the cauda equina causes loss of function of the lumbar plexus (nerve roots) of the spinal
canal below the termination (conus medullaris) of the spinal cord.

P/E

1. Inspection
Observe erythema infection/ long term using heating element
Skin marking café-au-lait-spots (NF)
 Hairy patches, lipomata (tethered cord)
 Dimples, nevi (spina bifida)
Posture level of shoulder and pelvis
symmetrical bone and soft tissue
Lumbar lordosis  exaggerated number characteristic of weakened abd wall

2. Neurological examination (lower extremities)

level Motor Reflexes Sensory

T12, L1,L2,L3 Iliopsoas- flexor hip - Anterior thigh
L2, L3, L4 Quadriceps- L2,L3,L4, femoral nerve Patellar- -
Hip adductor- L2,L3,L4, obturator nerve L3,L4
L4 Tibialis anterior- inversion of ankle Patellar Medial side of leg
L5 Extensor hallucis longus- dorsiflex great toe - Midline dorsum of foot
S1 Peroneus longus & brevis- eversion foot, Achilles Lateral side of foot
plantarflexion

3. Special test
a) Test to stretch spinal cord/ sciatic nerve
o Straight leg raise
o Cross leg (dorsiflex the foot)
o Kernig test
b) Test to increase intrathecal pressure
- Valsalva maneuver pain indicate lesion pressin on thecal sac
c) Test to stress sacroiliac junction (FABER)
- F-flexion
- AB-abduction
- ER- external rotation
Diagnostic tools

Laboratory Screen infection, cancer, spondyloarthropaties

No evidence in <7 w except in red flag
*ESR,CRP,WBC, HLA-B27, Tumor marker
Radiographs Osteoarthritis most common diagnosed
3 views
Indication hx trauma with persistent pain, 20<age>55 severe pain, spinal
deformity on PE, S&S of spondyloarthropathy , infection/tumor
Electromyelogram Measuring muscle function
Not appropriate for radiculopathy that clinically obvious
Bone scan Sensitive not specific
For malignancy screening, detect early infection or fracture
Myelogram Inject contrast material into spinal cord
CT myelogram Better than myelogram
For detail anatomical in multilevel disease in pre-op
determine nerve root compression
CT Bony bone changes of spinal/foraminal stenosis
Also fracture, degenerative joint disease, malignancy
MRI Diagnostic tool for
 Soft tissue abn infection, BM changes, spinal canal n neural foraminal
 Emergent cauda equine syndrome, spinal cordd injury, vascular
occlusion, radiculopathy
 Benign vs malignant compression
 Osteomyelitis
 Prior spinal injury

Treatment

Pharmacological Physical therapy Injection Surgery

1. NSAID 1. Electrical 1. Epidural steroid 1) Laminectomy
2. Muscle relaxents stimulation injection 2) Hemilaminectomy
(myofascial/muscular 2. Postural education -radiculopathy not 3) Discectomy
pain) 3. Massage/mobilizati respond to conservative 4) Fusion-
3. Membrane on/myofascial -small improve up instrumented/non
stabilizerTCA release months 5) Minimally invasive
4. Narcotics morphine 4. Stretching, exercise -less efficient in spinal spine surgery (MISS)
5. Steroids  in radiculitis 5. Traction stenosis -kyphoplasty
6. Tramadol 2. Facet block -percutaenous disc
3. Trigger point compression
4. SI joint
Cervical disc herniation
- 2 most common disc to herniate are C5-C6, C6-C7
- Next most common C4-C5
- Rare C7-T1

1) C4-C5 (C5 nerve root)

- Weakness in deltoid muscle
- Cause shoulder pain
- Not usually cause numbness and tingling
2) C5-C6 (C6 nerve root)
- weakness in biceps
- wrist extensor weakness
- numbness and tingling radiate to thumb side
3) C6-C7( C7 nerve root)
- Weakness in triceps
- Weakness of extensor muscle
- Numbness and tinglin radiate to middle finger
4) C7-T1( C8 nerve root)
- Weakness in handgrip
- Numbness and tingling down to little finger

Investigation
- X-ray  chronic degenerative changes, mets, infection, spinal deformity
 Not showing herniation
- CT scan  with myelogram
 In fracture, trauma
- MRI diagnostic
- EMG& Nerve conduct velocity

Treatment
- Anterior cervical discectomy and fusion, anterior cervical corpectomy and fusion
- Artificial disc replacement
- Key-hole laminoforaminotomy
- Laminectomy, laminoplasty
- lateral mass fusion
side notes from round

cushing triad for spinal injury

1) Bradycardia  parasympathetic overriding
2) Hypotension cut of sympathetic chain  give IV
3) Irregular respiration paralysis of diaphragm at C3,C4,C5

Criteria to differentiate between stable an unstable fracture

1) Ht. of vertebra lost > 50%
2) Subluxation
3) More than 2 column disrupted

Unstable treatment:
- Realignment
- Fixation
- Decompression

Stable treatment
- Immobilize for 3 month or walk with brace
Congenital anomalies of CNS

1. Craniosynostosis

-Premature fusion of cranial sutures abnormal skull shape

-20:80 syndromic:nonsyndromic
Types
a) Scaphocephaly
 Fusion of sagittal suture
 Bilateral expansion impaired
 Brain expand anteriorly and posteriorly
b) Trigonocephaly
 Metopic (bi frontal expansion impaired)
 Cause 2ry facial abn and vision problem
c) Brachycephaly
 Fusion bilateral coronal suture
 No anterior expansion
d) Plagiocephaly
 Unilateral coronal synostosis
Sign and symptom Dx:
1) Early fontanel closure 1) Skull 3D x-ray
2) Change shaped of head 2) Skull 3D CT scan
3) Palpable ridge of calcified fused suture
4) Orbital & facial abnormalities Treatment
 hypo/hypertelorism, exophthalmia Conservative: mild case/ plagiocephaly
5) Delayed IQ and development Surgery: 6 month, worst after 1 year
6) Strabismus, amblyopia
7) Inc. ICP

2. Arachnoid cyst
Developmental lesion arise from
splitting/duplication of arachnoid membranes
Types with sign and symptom
 Convexity  headache, adjacent
bone bulging, seizure
 Sylvian headache, seizure
 Suprasellar obstructive
hydroceph, visual abn, hormonal
def.
 Posterior fossa obstructive
hydroceph, brain stem dysfunction

Treatment
- Symptomatic followed up with regular MRI
- Surgically craniotomy and cyst wall resection
3. Hydrocephalus

Abnormal CSF accumulation in ventricles Types and Pathophysiology

Normally:
Production choroid plexus
Absorption  arachnoid granules
 Increase production: choroid plexus tumor
rare
 Circulation obstruction: tumor, cyst, post
hemorrhage/infarction, aqueduct stenosis
obstructive/ non-communicating
 Decreased absorption: fibrosis of
arachnoid due to hemorrhage/infection,
inc. venous pressure
communicating

Diagnostic Sign and symptom

Antenatal USG, MRI  Tense, bulge fontanel
Postnatal brain USG, CT scan, MRI  Inc. head circumference
 Prominent scalp veins
Treatment  Sunset eye
1) shunting  Transparent illumination of skull
2) endoscopic 3rd ventriculostomy  Dec. LOC
 Vomiting

4. Chiari malformation
- brain tissue extends into your spinal canal
Types:
Type 1 caudal displacement of cerebellar
tonsils into foramen magnum

Type 2 cerebellar+ inferior vermis+ 4th

ventrical herniate through foramen magnum
 Usually associated with
myelomeningiocele
Treatment
 Surgery: posterior fossa
decompression

Sign and symptom

 Most common occipital/cervical pain, inc by sneeze,cough, valsalva maneuver
 Brain stem nuclei dysfunction, cerebellar dysfunction, lower cranial nerve deficit(
nystamus, diplopia, dysphagia, dysarthria)
 Respiratory center dysfunction apneic spell
 5. Dandy Walker malformation

 4th ventrical cystic dilatation

 Vermis/ cerebellar aplasia
 Upward displaced tentorium
S&S
 75% with hydrocephalus
 Macrocephaly
 Delayed development
 Sign of inc. ICP
 Other have CNS and systemic abn.
Treatment
 4th ventricle peritoneal shunt/ + lateral
ventricular
 ETV Endoscopic third ventriculostomy

Neural tube defect (dysraphism)

Cranial anencephaly, encephalocele
Spinal spina bifida occculta ( tethered cord, split cord malformation)
spina bifida aperta (meningocele, myelomeningiocele)

Risk factor
1) Folic acid deficiency  3 month preconception
2) Family hx
3) 1st baby
4) Trisomy baby
5) Maternal DM, obese
6) Chemical, drug exposure  medication cessation that cross placenta
7) Radiation

 Encephalocele
- Herniation of brain tissue through defect in dura and skull
- Posterior (most common) and anterior
 Myelomeningiocele
- Herniation of meningeal sac filled with CSF and neural tissue
- Not covered with skin
- Sx of paraparesis, paraplegia, incontinence
- Increased in low socioeconomic status, white race
- Dx USG in 18-20 week, alpha-fetoprotein 16 week, acethylcolinesterase and MRI
- Prognosis 20% survive at 2yr in untreated, 80% at yr in treated

 Meningiocele
- Herniation of meningeal sac filled with CSF and neural tissue
- With intact skin
- Sx often absence or mild Dx fetal USG, MRI, postnatal MRI
- Mx: surgical repair

 Tethered cord syndrome

- attachments of spinal cord to dura that
- limit the movement of the spinal cord
- within the spinal column
- S&S: skin stigmata hair, dimple, discoloration
: motor and sensory deficit, incontinence,
Scoliosis
- Surgery by cord release

 Split cord malformation  Dermal sinus tract  Lipomyelomeningiocele

- Separation of cord into - Remnants of dermis - Fat tissue remnant grow
2 hemicord by fibrous from a failed separation in spinal cord/ dura
band/ bone spur neuroectoderm after - Sx of tethering
- Sx related to tethering neural tube closure
effect - 2ry infection
meningitis
Brain Tumors
Presentation
1. VISUAL symptoms due to:
- direct effect on optic nerve
- very high ICP
2. Headache
3. Progressive neurological deficit (motor,sensory or cranial nerve involvement)
4. Nausea and vomiting
Vomiting centre=Area Postrema (junction of medulla o. with SC)
Drugs, high ICP, anything will stimulate this centre
5. Seizure (mechanism-irritation of adjustment cortex)
6. CVA like symptoms due to:
- compression
- apoplexy (hemorrhage inside tumor)
7. Decrease level of consciousness
8. Constitutional symptoms (mainly in secondary metastases)
9. Behavioural changes
Headache Type of Headache in Brain Tumor
>Pain sensitive structure in skull: > Any type (migraine, tension, cluster)
1- Meningitis > Mainly due to
2- Soft tissue -High ICP : early morning headache
3- Facet joint 2 mechanisms:
4- Periosteum 1- Distribution of fluid when lying supine
5- Blood vessels (inc blood flow to tumor lead to edema around tumor)
2- Vasodilatation of CO2 retention
(deep sleep=respiratory centre depressed  accumulation
> Pain sensitive structure in brain: CO2  pCO2= major vasodilator  inc blood flow to
- It’s an Insensitive structure tumor=edema)
*IMPORTANT
Most common brain tumor – Metastasis
Most common primary intra axial tumor – GBM
Most common primary intra axial posterior fossa tumor- Hemanioblastoma (after ruling out mets)
Most common primary extra axial tumor – Meningioma

Most common tumor in children – AML (in general)

Second most common tumor in children – Solid brain tumors

Adults tumor usually Supra-tentorial

Children usually Infra-tentorial
Most common infra-tentorial tumor in children – Pilocytic Astrocytoma

Most common malignant midline tumor around $th ventricle

1- Medulloblastoma (from roof of ventricle)
2- Epyndymoma (from floor of ventricle)
3- Brainstem Glioma

Sellar Tumors – Pituitary or Meningioma (Adult)

- Craniophryngioma (Children)
Most cause for deep Intracerebral Hemorrhage – Hypertension
Causes for superficial ICH – Tumor
- Vascular (aneurysm, AVM,..)

GLIOMAS
-Group of primary tumor
-Composed of malignant glial cells
-E.x: -Astrocytoma
-Glioblastoma Multiforme
-Ependymoma
-Oligodendroglioma
-Medulloblastoma
ASTROCYTOMA
- Characteristic:
> slow growth
> cyst formation
> invasion of surrounding structures
> development of highly malignant glioblastoma within tumor mass

- Rx:
> Surgery
> Radio  post op or if Sx not possible (Temozolamide)
PILOCYTIC ASTROCYTOMA (Grade I)
- Children - C/P for cerebellar sign:
- Site: Supratentorial (Optic chiasm, Cerebral hemisphere) 1) Ataxia
Infratentorial (Children- optic nerve cerebellum 2) Dysmetria
hemisphere) 3) Intention tremor
- Macroscopic features: 4) Scanning dysarthria (jerky,explosive speech)
> Unencapsulated 5) Dysdiadochokinesia
> Well circumscribed 6) Nausea & Vomiting (w/out warning after positional
> Heterogenous mass change)
> Mural nodule associated with cyst If w/out preceeding nausea- suggest post fossa lesion

- Rx: Surgery 7) Obstruction of 4th ventricle secondary

hydrocephalus
 DIFFUSE ASTROCYTOMA (GRADE II)
- Young adult (20-40 y/o) - Risk for malignancy
- Site: Junction between frontal, parietal, >undergo malignancy within time
temporal lobe (dedifferentiation)
- Most common C/P: SEIZURE > Age (first decade or >50 y/o)
- Pattern: FIBRILLARY (most common) > > Size
Protoplasmic >Gemistocytic (worst prognosis) > Gemistocytic type
-MRI: - T2 hyperintense lesions > Increased enhancement
- Little or no
(enhancement, edema, hemorrhage)
- Rx: observe seizure, surgery
Radio or chemo
ANAPLASTIC ASTROCYTOMA (GRADE III)
- 40 to 60 y/o
- Cccs: Cystic/contain hemorrhagic foci/ calcification

GLIOBLASTOMA MULTIFORME GBM (GRADE IV) Any suspension of brain mass order:
- Age >50 y/o - CT: better for hemorrhage and calcification
- Most common primary Intra axial brain tumor - MRI: for details of soft tissues
in adult
- C/F: Inc. ICP - CT:
Seizure > Heterogenous mass
Focal Neurologic symptoms > Central necrosis
- Sites: Deep white matter > Ring enhancing (T1 w contrast)
Deep grey matter (paraventricular)
- Spread: White matter fibres (corpus callosum) DDx ring enhancing lesion:
Compress both frontal lobe butterfly - Abscess, GBM and metastases
glioblastoma
1ry: most common Rx:
2ry: malignant transformation from lower grade - Radio/chemo
- Surgical resection ASAP lead to wounded
glioma syndrome
PLEOMORPHIC XANTHOASTROCYTOMAS SUBEPENDYMAL GIANT CELL ASTROCYTOMAS
(GRADE II or III) ( GRADE I)
-Superficially located (temporal lobe) - Associated with Tuberous Sclerosis
-originate from subpial astrocyte - Triad:
- microscopic feature: large cell with eosinophil > Mental retardation
cytoplasm + lipid droplet , neuclear > Seizure
pleomorphism > Facial angiofibroma
- Common C/P: SEIZURES - Origin: Foramen of Monro (causing CSF flow blocked)
- DDx: Meningioma
OPTIC GLIOMAS BRAINSTEM GLIOMAS
- more common in children <20 yr - Signs and symptoms:
- Sporadic vs NF1 1) CN: may have CN palsy
- Sporadic(multifocal) involve optic chiasm 2) Long tracts signs: Hyperreflexia, Babinski sign,
- NF1 sparing optic chiasm urinary symptoms (frequency, urgency)
- Near hypothalamus, may extend to it  3) Secondary hydrocephalus
Endocrinopathies( precocious puberty, DM) 4)Involve cerebellar hemisphere
- Gelastic seizures: acute involuntary laughter 5)ataxia
(common with hypothalamic hamartomas )
- C/P: 4 growth pattern (MRI)
>most common presentation: Painless proptosis - DIFFUSE: most common (anaplastic
>visual loss astrocytoma)
>visual defects - CERVICOMEDULLARY
>inc ICP symptoms - FOCAL
> diencephalic syndrome - DORSALLY EXOPHYTIC: Pilocytic astrocytoma or
- Rx: for aggressive tumor gangliogliomas (histopathologically)
> Radiotherapy:
# >5y/o - CT: Non enhanced (except exophytic
# Tumor located other than intraorbital (chiasma component)
or retrochiasmal) If enhanced,, DDX High Grade Vermian Astrocytoma

# Sx not possible -Bad prognosis

> Chemotherapy: <5y/o - Rx:
> Medical ( corticosteroid) and radiotherapy
> surgical resection + biopsy
> Sx to confirm Dx (obstruction hydrocephalus or
dorsally exophytic type)
OLIGODENDROGLIOMA (GRADE II OR III)
- Adult (mostly MALE) 30-50 yo
- Child 6-12 yr in thalamic
- overexpressed of EGFR
- Initial presentation: Seizures
- Cause Intra cerebral Hemorrhage

1) Superficial Hemorrhage
> in the lobes (frontal*most common*, temporal, parietal)
> common cause: Trauma
> spontaneous causes: Extensive hemorrhage, structural causes

2) Deep Hemorrhage
> around thalamus and basal ganglia
> common cause: Hypertension
> most common site: Putamen Nuclei (basal ganglia)
- CT scan:
Anything white:
 Hemorrhage
 Calcification physiology/pathology
DDx:
1- Astrocytoma
2- Epyndymomas
3- Choroid Plexus
4- Craniophrangioma
5- Meningioma
6- Infection (hydatid cyst), meningitis, encephalitis
7- Vascular (giant aneurysm)
8- ArterioVenous Malformations AVM

Mass lesion causing midline shift

- Oligodendrioma
- Metastasis
- Meningioma

MENINGIOMA
- Most common primary extra axial tumor in adults- usually female (arise from arachnoid cap)
- Mostly benign
- Multiple more in NF2>NF1 (Adult)

In Children
-Most common site: Infratentorial (Intraventricular and posterior fossa )
- Associated with NF1

-Location
1) Parasagittal (most common location)
3 areas depending on tract of Superior Sagittal sinus (origin: Crista galli; Termination: Int Occipital
Protuberance)
> Anterior: Crista galli to Coronal suture
# present with frontal lobe symptoms – bilateral headache
- Apathy
- Urinary Incontinence
- Grasp reflex
- Behavioural changes
> Middle: Coronal suture to lamdoid suture
# Most common location
# Most common presentation – Jacksonian seizure and contralateral weakness (UMN lesion)
> Posterior

2) Convexity
3) Cerebellopontine angle
# Most common tumor here :
i. Acoustic schwanoma
ii. Sagittal meningioma
iii. Epidermoid cyst

-Main blood supply: Meningeal artery (ext carotid artery)

EXCEPT
Olfactory Groove Meningioma
Internal Carotid
Intraventricular Meningioma Branches
Tentorial meningioma

Ant Ethmoidal artery Supply

Ophthalmic Olfactory
artery Groove
Post Ethmoidal artery Meningiomas

Olfactory Groove Meningioma

- Embolization is contraindicated (complication: dissection of ophthalmic arteryBlindness)
- Foster Kennedy Syndrome (Medial Sphenoid wing meningioma can cause this syndrome)
Triad: 1) Ipsilateral anosmia
2) Ipsilateral optic disc atrophy
3) Contralateral papilledema

- Investigation
1- Skull Xray – calcification
- Hyper ostesis for adjacent bone localized skull thickening ( benign longstanding tumor)
- Groove of blood vessels
2- CT scan- calcification
3- MRI brain
4- Angiogram- involvement of sagittal sinus (tumor in parasagittal can obstruct this sinus- venous
infarction)

-Treatment
1- Not symptomatic- Incidental finding on MRI  Follow up for 6 months  no increase in size 
Follow up for 2-3 years
2- Embolization before Sx – decrease blood supply to tumor
3- Surgery – for symptomatic or increased in size
4- Radiosurgery – tumor in critical area of brain
PRIMARY CNS LYMPHOMA
- Non Hodgkin B cell lymphoma
- Inc. frequency in immunocompromised pt
-C/F: - Multiple cranial nerve deficits
- Uveitis
- Site: Multiple lesions
> Grey matter nuclei (usually deep, around ventricles)
> Basal ganglia
> Thalamus
 Cccs: - Ghost tumor (disappear with steroids)
- May resemble meningioma (ddx) but no calcification
- Ring enhancing lesions on MRI
-Treatment: Chemotherapy and Radiotherapy
HEMANIOBLASTOMA Von Hippel Lindau
- Any mass in post fossa is mets until proven - Autosomal Dominant
otherwise -Most malignant tumor involved: Renal cell Ca.
- Most common primary intra axial posterior fossa (might see hemanioblastoma or
tumor in adult (after ruling out mets) pheochromocytoma)
- Sporadic vs linked to Von Hippel Lindau
-Cccs:
> Cystic lesions with mural nodule
> like pilocytic astrocytoma in children but located
more superficially and dorsal

-C/F:Cerebellar lesion signs (ataxia,dyscoordination)

CEREBRAL METS
- Grey-white matter junction
- Mainly supratentorial
- Cccs: Extensive inflammation and edema (usually mets)

- Hemorrhagic metastatic tumor:

> Lung cancer (most common)
> Choriocarcinoma (highest tendency to bleed)
> Renal Cell Carcinoma
> Melanoma

- Inv: T2 MRI
- Treatment: Steroid, Mannitol, Lasix and Anticonvulsant (superficial tumorseizure)
CHOROID PLEXUS PAPILLOMA ** Communicating hydrocephalus:
- Causes both type of hydrocephalus (communicating and non- 4th ventricle dilated (if not=
communicating) obstructive hydrocephalus)
- Mechanism: - Obstruction
- Choroid plexus act as emboli (fluffy edges lead to ** Most common cause of
microemboli) communicating hydrocephalus:
- Papilloma increases CSF production  Infection (meningitis and
- Site – Children – Supratentorial (Lateral ventricle at Frontal encephalitis)
horn)
- Adult – Infratentorial (Rare)  Bleeding (IVH and SAH)

Spinal Tumors

Extradural- Metastasis (most common)

Intradural Extramedullary- Meningioma
- Schwanoma
Intradural Intramedullary- Astrocytoma
- Ependymoma
Neuromedicine
Headache
Hx:
 Site- unilateral/ bilateral, behind the eye/ radiate from neck
 Onset- begin suddenly and reach maximal intensity after short time/ gradually over minutes or hour
 Characteristic- throbbing, pressing, stabbing, squeezing
 Associated: N&V, sensitive to light/sound, flashing light,paresthesia, weakness, difficulty with
concentration/speech
 Time: lasting for few minutes, hours, days, persistent, frequency of attack
 Exacerbation/relieving: by activity, by rest

P/E:
 Complete neuorological examination
 Papilledema  increase ICP
 Temporal arteries tenderness giant cell arteritis
 Neck stiffness meningitis
 Blood pressure, carotid bruit, murmer

Investigation:
 ESR, KFT,LFT,TFT
 Lumbar puncture
 Fundoscopy
 CT/MRI

Red flags of headache

1. Age extremities
2. Diurnal variation  morning sign of inc ICP
3. Severitysuperacute in SAH
4. Association vomiting, unrine incontinence, LOC,(neurological deficit) vertigo
5. Positive meningeal sign
6. Chronic headache
7. Know case of malignancy

Types:
Primary Secondary
 Migraine  Mass
 Tension type  Increased ICP
 Cluster  Inflammation
 Paroxysmal  Infection
1ry headache

Migraine headache
2nd most common cause if headache Types:
S-unilateral 1) auraflashing/ zig-zag line (scintillating scotoma),
C- throbbing, pulsating tempo-marching/progressing across visual field over
A- nausea an vomiting 5-20 min
T- last from several to 72 hr 2) without aura
E- increase by movement,light, sound

Mx:
 Prophylactic b-blocker, TCA, anticonvulsant
 Abortive( alleviate headache during attack) triptans
 Patient with meniere’s disease Acetozolamide

Tension type headache

Most common
S- recurrent attack of bilateral/holocranial
C-pressuring, tightening, squeezing, tightening
T- 30 min to several days
A- not associated with nausea& vomiting
E- not increase by exercise or activity

Cluster headache
Known as trigeminal autonomic cephalgias (TCA) Mx: Triptans,
 Unilateral trigeminal nerve pain Oxygen
 With ipsilateral autonomic symptom  Ordinary
S- unilateral, orbital or temporal region painkiller
C- excruciating not very
A-cranial autonomic symptom  lacrimation, conjunctival injection, effective
facial/forehead swelling, eyelid edema, nasal congestion, rhinorrhea, and
horner syndrome
 Pt also feel restless
T- high frequency, last days, weeks or month
E- improves by moving around

Paroxysmal hemicranias
S-unilateral
T- shorter from cluster but with greater frequency
A- Accompany with autonomic symptom
R-relieved by NSAID  INDOMETHACIN
2ry headache
Subarachnoid hemorrhage
Idiopathic intracranial hypertension
Temporal arteritis
Chronic daily headache
Trigeminal neuralgia
Postherpetic neuralgia
-worst headache in life
-sudden and peak intensity within short time
-known as thunderclap headache
-dx by CT and LP
-increase pressure within subarachnoid space
-increase in recumbent, vasalva maneuver and relief in
upright position
-worse in morning
-associated with pulsatile tinnitus and transient visual
disturbance
- Ix: papilledema, unilateral/bilateral sixth nerve palsy
-affect young overweight women
-etiology: impaired resorption of CSF
-cx: visual loss
-known as Giant cell arteritis
-affect medium and large artery
- more in 50s
-associated scalp tenderness, thick, nodulation,
tender of temporal arteries
 fever, wt loss, fatigue
-cx: visual los s
-ix: ESR,CRP, biopsy of temporal artery
-mx: high dose steroid
-present almost every day/ at least 15 days per month
-causes are from 1ry an 2ry headache
-most common chronic tension type, medication
overuse, withdrawal sx
-paroxysms of severe neuropathic pain in one or more
branches of 5th nerve
-short, electric-like painful sensation in face
-triggered by combing hair, brushing teeth, eating,
shaving
-mx: carbamazepine
-after acute attack of shingles
- re-activation of dormant infection in dorsal root of
ganglion
-burning, itching, hypersensitive to light
-early treated by acyclovir
-on present TCA, gabapentin
Stroke
- Rapid focal cerebral dysfunction lasting >24hr or lead to death cause by vascular origin
- Classification:
1) ischemic  thromboembolism and hemodynamic failure
 inadequate blood flow death of brain cell stroke
2) hemorrhage
- Movement, sensation emotion in affected area are lost in function or impaired
- Varies in severity by location and extend of damage

Risk factor
Modifiable Non-modifiable
- Atrial fibrillation * - -age
- HTN - -gender> women
- Asymptomatic carotid stenosis - -race> African
- DM - -heredity
- Hyperlipidemia
- Obese
- OCP
- Sickle cell disease
- Smoking

Etiology and pathophysiology

- Brain need continuous supply O2 and glucose
- If blood is interrupted  neurologic metabolism altered in 30 sec
 Metabolism stops in 2 min
 Cell death in 5 min
- Atherosclerosis is major cause of stroke  thrombus emboli
- Border zone around core area of ischemic is potentially reversible
- Restoring blood flow < 3hr can lessen damage

TIA ( Transient Ischemic Attack)

- Temporary focal loss of neurologic function because of ischemia
- Resolve within 3hr
- Micro-embolic that temporary block blood flow
- Warning sign of progressive cerebrovascular disease

Emergency diagnosis (FAST)

F- face  drop face, ask to smile
A- arms one arm weak/numbness, ask to raise hand
S- speech slurred, ask to repeat simple sentence
T- time call 911
Ischemic stroke

- Inadequate blood flow to brain due to partial/complete occlusion of artery

- 85% cases
- Most pt not have decreased LOC in first 24hr
- Sx worsen first 72hr  cerebral edema
Thrombotic Embolic stroke
- 2/3 with HTN and - embolus lodge and occlude CA
DM - infarction and edema in area supplied by the vessel
- Preceded by TIA - 2nd most common cause
- Emboli mostly from heart
- Sudden, rapid occurrence of severe clinical sx
- Remain conscious + headache
- Recurrence is common

Hemorrhagic stroke
- 15% of all stroke
- From bleeding into brain tissue/subarachnoid space/ ventricles
Intracerebral hemorrhage Subarachnoid hemorrhage
- Bleeding in brain caused by rupture of vessel - Bleeding in CSF
- HTN is most common cause space
- Occur during activity - Cause by rupture
- Sudden, progressive over min to hr aneurysm
- Neurological deficit, headache, N&V, decreased LOC, HTN
 Clinical manifestation

Motor function Communication Affect

Impaired: Aphasia total loss of  Difficult controlling emotion
- Mobility comprehension and use of  Response may exaggerated/
- Respiratory language unpredictable
- Swallowing and speech Dysphasia difficult with  Depression
- Gag reflex comprehension and use of  Frustrated by mobility and
- Self care ability language comprehension problem
Contralateral Dysarthria  disturb muscular
 Loss voluntary skill that control speech
 Impaired integration of impaired pronounce,
movement articulation, phonation
 Altered muscle tone: NOT meaning/comprehension
flaccid to spastic
 Altered reflexes: hypo to
hyper
Intellectual function Spatial perceptual alteration Elimination
 Impaired memory and  Deny illness or body part  Initially and temporary
judgment  Erroneous perception of self  Prognosis normal bladder function
 Memory problems related in space ( neglect all input excellent when only one hemisphere
to language in left brain from affected side) affected
stroke  Inability to recognize object
 Inability to carry command

Acute care

1. Assessment findings

- Altered LOC
- Weakness, numbness, paralyse
- Speech/visual disturbance
- Severe headache
- Abn heart rate
- Respiratory distress
- Dilated pupil
- HTN
- Facial drooping
- Difficulty in swallowing
- Seizure
- Incontinence
- Nausea, vomiting
- vertigo
2. Intervention

a) Initial:
- ABC
- Maintain BP
- IV access
- Immediate CT scan ischemic vs hemorrhage
- Control ICP
- Prophylactic seizure
- Avoid hyperthermia  inc. cerebral metabolism
b) Thrombolytic/ fibrinolytic + tPA  reestablish blood flow and prevent cell death in ISCHEMIC stroke
give within 4-5 hr to reduce disability
24 hr after tPA give antiplatelet, anticoagulant
maintain therapeutic level (INR, PTT)
c) Ongoingmonitor vital sign an neurologic status  10-15% will have seizure in 24 hr
d) Surgical  evacuate any hematoma, clip/wrap/coil any aneurysm

3. Rehabilitation

- After stabilize 12-24 hrlessen disability and attaining optimal function

4. Planning

- Maintain/ improved LOC

- Maximizing physical function
- Maximizing self-care abilities and skills
- Maximizing communication abilities

Prevention
A- antithrombic/ anticoagulant Antiplatelet drugs Surgery
 Aspirin, clopidogrel,  Aspirin  Carotid endarterectomy
Aggrenox, warfarin  Transluminal angioplasty
B- blood pressure control  Stenting
C- cholesterol, carotid  Extra-intracranial bypass
revascularization
D- DM control
MULTIPLE SCLEROSIS (scars)
What? Etiology
- Demyelination of insulating covers of nerve  Chronic Infections
cells in brain and spinal cord  Viral infections(common cold, influenza,
- Disease of UMN (PNS rarely involved) GE) can increase the risk
- T & B cells disease  Stress
- Begins at age 20-50 y/o  Genetics
-Female > male  Geography  northern European

Pathology
- Multiple plaques or lesions affecting commonly white matter
- Tendency to affect some areas more:
 Periventricular white matter
 Juxtacortical
 Corpus callosum
 Infratentorial: brainstem, cerebellum
 Spinal cord
*white matter function to carry signals between grey matter where processed is done
Hallmark:
1- Dissemination in space: more than one area
2- Dissemination in time: [clinical course]
Signs and symptoms
Charcot-Triad of MS
- Scanning speech
- Nystagmus
- Intention tremor

Specific
- Vision problem: Double vision (diplopia),
optic neuritis(unilateral)
- Inter Nuclear Ophthalmoplagia :
Impaired horizontal eye movements,
usually bilateral (Unilateral=Stroke)
- Muscle weakness
- Sensory changes (numbness, tingling)
- Coordination problem: ataxia
- Partial transverse myelitis or Clinically Isolated Syndrome (60% dev into MS in 10 years)
Others
- Very pronounced reflexes
- Muscle spasms or difficulty in movement
- Problem in speech or swallowing
- Bladder or bowel difficulties
- Depression or unstable mood
- Uhthoff phenomenon: worsening symptoms due to exposure to higher than usual temperature
- Lhermitte phenomenon: electric shock sensation when neck is flexed (effect of demyelination in SC-
not specific for MS)
Clinical course:

1. Relapsing-remitting
- Rapid onset relapses followed by months or years of partial or complete recovery
- Signs and symptoms suggestive demyelination process presence at least for 24 hours in the absence
of fever or infection
- Deficits during attack can either
 Resolve or leaving problems in about 40%
 The longer the person had the disease, the more common the deficits
- If deficits always resolve between periods = Benign MS
2. Primary progressive
-Age around 40 y/o
- Insidious onset, progressively deteriorate over time
- Typically present as progressive myelopathy (rarely as brainstem or cerebellar syndrome)
- MRI lesions
 Fewer in number
 Less likely to enhance with gadolinium (compared to relapse-remitting)

3. Secondary progressive
- Up to 40% relapsing-remitting become progressive after 20 years
- Dx: When patient demonstrates progression independent of relapses at least 6 months
- Deterioration of:
 Gait
 Balance
 Spasticity
 Bladder function
 Cognitive declines

4. Clinically Isolated Syndrome

- 85% begins as CIS
- 45% have motor or sensory symptoms
- 20% have optic neuritis
- 10% have symptoms related to brainstem dysfunction
- 25% have more than one difficulties

Treatment with Interferon decreases chances to progress into MS

Diagnosis

MacDonald Criteria: Clinical, Lab and Radiologic evidence of lesions at different times and in different
areas

- MRI: golden standard

- Electrophoresis of CSF fluids: Oligoclonal bands of IgG (inflammation marker found in MS)
- Evoked potentials: check brain responses to stimulation of optic and sensory nerves

Treatment

1) Steroids- IV methylprednisolone
- High dose in acute attacks for 3-5 days
- if lack recovery  2nd line

2nd line:
2) Plasmapheresis
3)Cyclophosphamide
4) IVIg (immunomdulators)

Disease modifying treatment (relapse remitting MS):

5)Interferon
- Beta 1a (Avonex) Low dose: IM weekly
 High dose: SC 3x/week
- Beta 1b (Betaseron)SC every other day
- fingolimod

6) Spingosine-1-phosphate receptor modulator

- inhibit migration of T cells from lymphoid to peripheral circulation and target organs

Side effect
- 1st dose bradycardia  herpes virus dissemination, macular edema, long term high BP
 6hr first dose observation
 Movement disorder
Definition
neurological motor disorder manifested by
-slowness/ poverty of movement (brady/hypokinesia)
-abnormal involuntary movement (hyperkinesia)
1. Tremor
-involuntary,rhythmic, and stereotyped oscillatory movement of body part from alternating
synchrounous contraction of antagonist muscle
Type
Rest tremor Parkinson disease
Postural tremor Physiological ,essential, dystonic, drug, metabolic, neuropathic
Kinetic tremor Cerebellar, rubral tremor

Physiologic tremor Essential tremor

 In healthy person  Most commom
 8-12 Hz  Worsen with age
 Aggaravated by  5-10 Hz
-stress, fatigue, emotions, hypoglycemia,  50% AD
hypothermia  Mild parkinsonian features
-thyrotoxicosis, pheochromocytoma, drug  Symmetric postural tremor in upper
withdrawal, alcohol, beta agonist limb(hand head voice)
 Improves with alcohol

Mx
Propanolol
Primidone
Benzodiazepine
Surgery: DEEP BRAIN STIMULATION
Parkinson disease
Causes: loss of dopaminergic neuron in substantia niagra pars compact
Factors: smoking, caffeine (protective)
family hx,concussion,migraine with aura,rural place, chemicals exposure,well water,diet ( risk)

Motor features
 Tremor (rest, pill rolling, re-emergent)
 Bradykinesia
 Rigidity
 Postural instability
Non motor features
 Cognitive dysfunction
 Psychosis
 Mood, sleep disturbance
 Fatigue
 Autnonomic, olfactory dysfunction
 Mx of Parkinson
 Levodopa
 Dopamine agonist
 Amantadine
 Monoamine oxidase B inhibitor
 Anticholinergic agents
 COMT
 Surgery

NOT Parkinson if
 early dementia
 early postural instability
 early hallucination and psychosis
 ocular sign (impaired vertical gaze)
 early autonomic syndrome
 alien limb phenomena
 prominent motor apraxia
 early marked symmetry
 truncal> appendicular

2. Chorea
-abnormal involuntary movement usually distal, brief, nonrhythmic, abrupt, irregular,flow from one part
to another

Ddx
 athetosis= slow flowing writhing involuntary movement
 ballismus= movement of proximal lim muscle with larger attitude and more rotatory

Causes: disruption of basal ganglia modulation of thalamocortical motor pathway (putamen, globus
pallidus, subthalamic nuclei)

Factors:
-AIDS
-genetic conditions, such as Huntington’s disease
-immune conditions, such as systemic lupus erythematosus
-infection-related conditions, such as Sydenham’s chorea
-medications, including levodopa and neuroleptics
-metabolic or endocrine disorders, including hypoglycemia
-pregnancy, known as chorea gravidarum
 Huntington disease Sydenham chorea
 AD  Group A beta hemolytic strep
 Cytosine-adenine-guanine expansion  5-15 yr
 4p 16.3  Rheumatic fever (few week after onset)
 Juvenile vs adult  + OCD
 Chorea, dementia, behavioral changes  Self limited
 20% recurrence

Mx
-no therapy
-monoamine inhibitors (deplete dopamine): tetrabenazine,reserpine
-antipsychotic (dopamine receptor antagonist): haloperidol, risperidone
-anticonvulsant :clonazepam, valproic acid

3. Dystonia
-hyperkinetic disorder which is involuntary, sustained muscle contraction causing twisting and repetitive
movement/abnormal posture
-simultaneous btw agonist and antagonist muscle

Classification
Age Anatomic distribution Etiology
 Young <26  Focal-single body part 1ry
 Late >26 -blephrospasm -familial
-oromandibular -sporadic
-spasmodic dysphonia 2ry
-cervical -heredodegenerative
-drug
 Segmental- 2 or more contagious -trauma
 Multifocal- 2 or more non contagious -structural lesion
 Generalized- segmental crural -psychogenic
dystonia
 Hemidystonia- one half body

Mx
-in focal give botulinum injection
-anticholinergic
-BDZ
-GABA agonist
-levodopa
-surgical
4. Wilson disease
-hereditary disorder of Cu metabolism
-characterized by abnormal accumulation of Cu in liver and brain lead to cirrhosis and neuronal degeneration
Etiology Presentation Ix
- AR  Hepatic injury/cirrhosis  slit lamp test for kayser
- ATP7B Gene on ch 13  Dysarthria, tremor, fisher ring eye
- reduced Cu binding to dystonia, bradykinesia  ceruloplasmin level
apoceruloplasmin   Cognitive change, reduced
ceruloplasmin anxiety, affective  24 hr urinary copper inc.
disorder  Liver biopsy
 Kayser fisher ring of eye
Mx
*consider in young pt with  Chelation therapy
unexplained tremor,dysarthria, -D-penicillin,trietrin, zinc salt
psychiatry/hepatic disease  Liver transplant

5. Tics
-sudden, quick, movement or sound that repeated at irregular interval

Types
Simple motor Simple vocal Complex motor Complex vocal
 Eye blinking  Sniffing  Touching  Repetition of word
 Nose twitching  Crunting  Throwing  Repetition of obscenities
 Head jerking  Throat clearing  Hitting  Repetition of part of
 Shoulder  Screaming  Jumping word
shrugging  Copropaxia  Repetition of other
 Abd muscle person word
tensing

Tourette’s syndrome
Presence of both motor and phonic tics Presentation
At least one year  Childhood
Fluctuation, frequency, severity  Motor before vocal tics
Before age 21 yr  85% reduced in tics during n after adolescence
 OCD, ADHD

Mx
1. Alpha agonist-clonidine, guanficine
2. Neuroleptic- risperidone, olanzapine, aripiprazole, pimizole, haloperidol, fluphenazine
3. BDZ- clonazepam
4. Botulinum injection
5. Tetrabenazine, pergolide, ropinirole
6. Myoclonus
-sudden, brief, shock-like involuntary movements

Types Mx
1. Physiologic – hypnic, anxiety, hiccup 1. Sodium valproate
2. Essential 2. levetricetam
3. Epileptic
4. Symptomatic

7. Tardive dyskinesia
- involuntary movement of tounge,lips,face,trunk and extremities
-occur in patient treated with long-term dopaminergic antagonist medication
Seizures and Epilepsy
- More common in children and elderly
Seizures Epilepsy
Temporary alteration in brain function due to excessive Disorder characterized by tendency
synchronized neuronal activity toward 2 or more unprovoked seizure
Causes
1. Children- lots of causes but will outgrow them after >20 yr
2. Elder- degenerative brain disease(alzheimer),
comorbidities( hypocalcemia,hyponatremia,
hypernatremia) , multi-infarct strokes, tumors
Recurrence rate 30-70%

1. Seizures
Partial simple Partial complex
No alteration of level of consciousness Altered level of consciousness ( not necesserily unconscious)
Depends on part of brain affected Associated with automatism( blinking eye, smacking lip)
a) Frontal lobe, precentral gyrus
= abn movement in hand or leg
=jacksonian march if spread over precentral gyrus
b) Temporal lobe
= gustatory feeling, uprising sensation of stomach,
abn taste/smell, déjà vu, jamias vu, hallucination,
fear, panic, euphoria
= impaired level of consciousness if spread into
contralateral lobes
= 2ry generalized seizure if spread to other lobes
c) Central cortex, postcentral gyrus
= sensory sx, tingling
Secondary generalized seizure Generalized seizure
- Proceed after partial seizure Both hemisphere involved at same time, Abrupt loss of
- Often with tonic-clonic seizure consciousness
Types:
a) Myoclonic
- Shortest, single/multiple jerks
*non-seizure myoclonus= sign of pulmonary failure,COPD
b) Clonic
- Rhythmic jerking
c) Tonic
- Sustained muscle contraction
d) Tonic-clonic
- Tonic period followed by clonic jerking
e) Absence
- <30 sec with eye fluttering/ some autonomic features
- 3 Hz spikes
f) Atypical absence
- Longer duration with more autonomic seizure
- EEG 1.5-2.5 Hz
 g) Atonic
- Loss muscle tone

2. Epilepsy
Idiopathic
a) Benign epilepsy with centrotemporal b) Juvenile myoclonic epilepsy (JME)
spikes (rolandic epilepsy) - Myoclonic movement in morning happened
- Genetic, family hx for years tonic-clonic
- Partial seizure  focus in - 1/3 +ve family hx
centrotemporal - Normal neurologically n developmentally
- In school aged resolve by puberty - Might have other type of generalized seizure
- Good prognosis - Long-life condition not outgrow it
- Presentation: nocturnal seizure(night), - Rx: valproic acid (boy), lamotrigine (girl)
excess saliva, gurgling, choking, clonic
upper face and upper extremities
- Rx: tergetrol (carbamazepine)/
lamotrigine

c) Lennox-Gastaut
- 1-10 years old
- Present with multiple seizure (tonic, atonic, atypical absent)
- EEG abnormal , more in sleep, 1.5-2 Hz
- Rx: broad spectrum anti-epileptic drug (falbamate)/ vaus nerve stimulator

Cryptogenic and Symptomatic

a) Rasmussen’s Encephalitis
- Also known as Epilepsia partialis
continua
- Ex. of partial seizure
- Childhood
- Presentation: frequent severe
uncontrolled focal seizure, loss motor
skill and speech, hemiparesis,
encephalitis, dementia
- Involves one hemisphere
- Causes: infection of virus
autoantibodies against GluR3
- Rx: hemispherectomy of effected
cerebral hemisphere
b) Temporal lobe epilepsy
- Ex. of partial seizure
- Due to mesial temporal sclerosis(
hippocampus) on coronal cut MRI
- Temporal lobe sx: rising epigastric
discomfort, nausea, fear, autonomic sign,
olfactory hallucination, loss of awareness
- Start in one sided consciousness
preserved intially
- Postictal phase
- Hx of prolonged seizure
 c) Frontal lobe epilepsy d) Infantile spasm
- Ex. of partial seizure - Has underlying problem  inborn error of
- Frequent and happen during 2nd stage metabolism, brain structural abn, tuberous
of sleep, short duration, sclerosis
- No postictal confusion - Bad prognosis
- Motor sx, brief, 10-40 sec, bilateral - Mental retarded
tonic-clonic - Presentation: jack knifing- sudden flex,
- Conscious preserved extense/mixed flex-extense of trunk and
- Other sx: bicycling asynchronous proximal muscle
bilateral movement -> confused with - Rx: ACTH, vigabatrin
pseudoseizure - EEG: high amplitude, sharp and slow
wave hypsarryhtmia

Provoke seizure
1. Metabolic abnormalities -
- hyponatremia * don’t rapidly treat central pontine myelinosis
- Hypocalcemia
- Hypoglycemia
- Hyperthyroidism
- Hypermagnesemia
2. Porphyria
3. Hypoxia
4. Medication: benzo, barbiturate withdrawal, bupropion, tramadol
5. Abuse substance: cocaine, amphetamine, phencyclidine, ecstasy
6. Eclampsia
7. Alcohol withdrawal

Alcohol withdrawal Eclampsia

 90% happen within 7-48 hr after cessation  Women with pre-eclampsia
 Occur up to 7 days after cessation  Sx: headache, blurry vision, confusion,
 Sx: tremourlousness, myoclonic jerk of hallucination
extremities  > 20 week GA to 4 week postpartum
 Cx: Delirium tremens, status epilepticus,  Rx: Mg SO4
falling down
 EEG
 Thiamine > glucose to prevent wernickes-
korsakeff encephalopathy(mammillary
body hemorrhage) , lorazepam, and
electrolyte abn
Febrile seizure
- Seizure + fever
- 6 m to yr
- 1/3 recurrence
- First day of fever
- Usually tonic/ tonic-clonic
- Complex if > 15 min, > 1 seizure in 24 hr, focal seizure (more prone to develop complex partial
seizure & epilepsy)
- Mx: identify lying disease LP if suspected meningitis
- Prolonged seizure use rectal diazepam

Mimics of seizure
1. Syncope – vaso vagal, neurosymptomatic, low CO, volume depletion, arrhythmia
2. Migraine- basilar type
3. Stroke, TIA
4. Sleep disorder- RBD, narcolepsy, cataplexy, parasomnia
5. Movement disorder- tics
6. Transient global amnesia
7. Psychiatric disorder

Workup for seizure

1. Hx: medication, drugs, previous seizure, myoclonus screening, loss of time, odd
behavior, staring spells,
2. Risk: febrile seizure, developmental delay, head injury, CNS infection, family hx
3. P/E: systemic disease/ skin
4. Labs: CBC, electrolyte, comprehensive metabolic panel( Ca, Na, K, Cl), Mg, urine drug
screen, Etoh level (alcohol withdrawal)
5. EEG
 Low sensitivity, high specificity should repeat
 3x of 30 minutes  sensitivity 90%
 Routine EEG last for 20 minutes, video EEG
 Hyperventilation, phonic stimulation, sleep ( slow wave, artifact muscle
movement) increase yield EEG
 Sleep deprived and come for test while sleeping more sensitive
 Distinguish partial/ generalized
6. MRI

Psychiatric comorbidities
- Depression in 40%
- 5-10x risk of suicide
- Anxiety, psychosis
Pseudoseizure
- Paroxysmal change of behavior  no organic causes, no EEG changes, an conversion disorder
- Comorbid psychiatric disorder/ abuse hx
- Monitored by video EEG
- Ddx frontal lobe seizure

Women vs seizure
*complication of antiepileptic drug
- Ovarian abn: PCOS, anovulation
- Induce metabolism of female sex hormone reduce efficacy of COC
- Fetal malformation(valproic acid)  use lamotrigine
- Osteoporosis and osteopenia

Status epilepticus
Abnormal state which seizure is continuous or so frequentthat no recovery for > 30 min
Mx:
1. ABC
2. IV, glucose fingerstick
3. Thiamine 100mg IV  50% dextrose
4. Lorazepam IV / rectal
5. If continues phenobarbitol and intubate
If continues induce coma with barbiturate, midazole/propofol & EEG monitoring continuously
PERIPHERAL NERVE DISEASE

- Diseases of LMN system and sensory (and autonomic)

- Share the common signs and symptoms but with different distributions depending on area involved
Signs and symptoms:
Motor  Weakness, change in muscle bulk, paralysis, abnormal movement
SensoryNumbness, tingling
AutonomicBradycardia/Tachycardia, postural hypotension, impotence, impaired sweating
LMN diseaseHypotonia, reduced reflexes, atrophy, fasciculations and flaccidity

Some terms used to describe patient’s condition:

Predominantly sensory neuropathy
Caused by: DM, thiamine deficiency, malignancy, amyloid, uremia, sarcoid, leprosy,
Predominantly motor neuropathy
Caused by: GBS (acute),lead, botulism, diphtheria, Charcot Maries Tooth, Lyme disease
Sensory-motor neuropathy
Autonomic neuropathy

Investigation for PND in general:

1- Clinically
2- EMG/NCS – axonal or demyelination
3- CSF cytoalbuminocytologic dissociation (elevated protein with <5)- in GBS
4- Special studies- Lyme PCR
5- Nerve biopsy in certain cases- vasculitis, Leprosy, Amyloid neuropathy, sarcoidosis

RADICULOPATHY
- Usually cervical or lumbosacral
- Symptoms
> Pain: Brachialgia (start in the neck radiating to upper extremity- cervical radiculopathy)
: Sciatica (start in lower back radiating to lower limbs- lumbosacral radiculopathy)
> Motor and sensory follows the distribution of affected root (ex: C7- motor symptoms in biceps and
sensory in C7 area)

-Causes:
> Compressive: Disc disease (most common), tumor, abscess
> Non compressive: Diabetes, Herpes Zoster
> Diabetic radiculopathy can affect thoracic region
- Diagnosis: Clinical, MRI of involved area, Electromyography and Nerve Conduction Studies
- Treatment according to etiology
PLEXOPATHY
-Usually brachial or lumbosacral plexus
- S&S (think motor,sensory)
- Causes:
> Compressive: Tumor- Brachial plexus (breast and lung tumor), Lumbosacral plexus (gyne and
colorectal tumor)
> Non compressive: Diabetes, Infections, Radiation induced plexopathy

- Diagnosis: Clinical, MRI of involved area, EMG/NCS

- Treatment according to etiology

MONONEUROPATHY
- Upper extremity: Median nerve (Carpal Tunnel Syndrome- most common), Ulnar nerve, Radial nerve
- Lower extremity: Peroneal nerve
1- Carpal tunnel syndrome
> Mostly bilateral
> Risk factors: Thyroid dysfunction, Rheumatoid arthritis, Pregnancy, Diabetes and Occupation
> Symptoms: Initially palmar pain, numbness and tingling in 3.5 lateral fingers, muscle weakness (FP,
AP. OP) and possibly atrophy
> Diagnosis: Clinical, EMG/NCS
> Treatment: Conservative – analgesic, local steroid injection
Surgical (if severe & not respond to treatment)

2- Ulnar neuropathy
> Compression at elbow (ulnar groove behind medial epicondyle)
> Symptoms: Sensory symptoms in medial 1.5 fingers, motor symptoms in muscle FCU, FDP,
Lumbricoides oppones
> Diagnosis: Clinical, EMG/NCS
> Treatment: Conservative, surgical

3- Radial Neuropathy
> Secondary to compression at spiral groove of humerus (Saturday night palsy)
> Symptoms: motor>sensory; weakness of wrist dorsiflexors (wrist drop)
> Diagnosis: Clinical, EMG/NCS
> Treatment: self-limiting with physiotherapy, if mass, remove it

4- Peroneal neuropathy
> Compression usually at fibular head
> Risk factors: Sudden severe weight loss, frequent leg crossing esp in thin people, driving with knees
touching gear side
> Symptoms: mostly motor- weakness of foot dorsiflexors (foot drop), sensory in peroneal
distribution
> Diagnosis: Clinical, EMG/NCS
> Treatment: Self-limiting with physiotherapy and AFO’s, if mass, remove it
POLYNEUROPATHY
> Classical polyneuropathy or peripheral neuropathy
> Starts distally and progress proximally, bilaterally
> Symptoms: sensory and motor, sometimes autonomic (depends on which nerve affected)
> Causes: (secondary)
- Systemic disease: DM (most common), Chronic hepatic or Renal failure, thyroid diseases,
infections(leprosy)
- Autoimmune
- Medications: Chemo therapy
- Toxins: Alcohol intoxication, drug abuse
- Nutritional deficiencies: B12, folate
- Hereditary causes: CMT
> Diagnosis: Clinical, EMG/NCS
> Treatment: according to etiology, treat neuropathic pain

After excluding 2ndary causes primary (AIDP & CIDP)

1- Acute Inflammatory Demyelinating Polyradiculoneuropathy = Gullain Barre Syndrome
 Preceed by URTI or GI infection
 Motor defect presentation (more)
 Ascending weakness lowerupper extremities (in less than 4 weeks)
 Reduced or absent reflexes (LMN signs)
 Involve Facial and Respiratory muscles
 Mx: Admit to ICU, follow up respiratory status (restrictive type) by PFT (ABG-it’s too late)
 Diagnosis: Clinical, EMG/NCS, CSF-cytoalbuminocytologic (high protein and lymphocytes)
 Treatment: Plasmapheresis, IVIg, Respiratory support (NO STEROID)

2- Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP)

Similar to AIDP but differ in:
 Progression of symptoms >8weeks
 1/3 have relapsing-remitting patterns
 Very responsive to steroids
 Motor and sensory symptoms with reduced reflexes
 Diagnosis: Clinical, EMG/NCS
 Treatment: IVIg, Steroids, Steroids sparing agents
MONONEUROPATHY MULTIPLEX
> Patchy involvement of multiple nerves
> Etiology: Vasculitis (most common), DM
> Symptoms: Sensory and motor, pain (prominent feature)
> Treatment: treat etiology and neuropathic pain
Treatment in general
Mx Neuroptahic pain:
Analgesics
Anti epileptic: Gabapentin, Phenytoin, Carbamazepine
Tricyclic antidepressants: Amitriptyline
Mexiletine
Local Anaesthetics: Lidocaine (or patches-containing lidocaine)
Codeine/Oxycodone
Mechanical Aids:
Hand or foot braces
Orthopedic shoes- improve gait disturbance and reduce injury in people with loss of sensations
Mechanical ventilation- if severely impaired
Surgery
Repair slipped disc, remove tumor, surgical release of ligaments or tendons (for nerve entrapment)

DDx of mononeuropathy is radiculopathy

Ex: - Peroneal neuropathy and L5 radiculopathy
- Carpal Tunnel Syndrome and Cervical radiculopathy (C6,7,8)
- Radial neuropathy and Cervical radiculopathy (C6,7)
- Ulnar neuropathy and Cervical radiculopathy (C8)
DDx of Neuropathies by clinical course
Acute onset Subacute onset Chronic course/ Relapsing/
(within days) (weeks to months) insidious onset remitting course
Guillain-Barré Maintained exposure to toxic Hereditary motor Guillain-Barré
syndrome agents/medications sensory syndrome
neuropathies
Acute intermittent Persisting nutritional Dominantly CIDP
porphyria deficiency inherited sensory
neuropathy
Critical illness Abnormal metabolic state CIDP HIV/AIDS
polyneuropathy
Diphtheric neuropathy Paraneoplastic syndrome Toxic

Thallium toxicity CIDP Porphyria

DDx PND
- Myelopathy
- Syringomyelia
- Dorsal column disorder (Tabes Dorsalis)