Pemicu 2 Saraf

Penurunan Kesadaran
LI 2
Pemicu 2
Tak Sadarkan Diri
Lidya Oktaviani Siauw
405140006
Tingkat kesadaran
LI 1
Definitions
• Conciousness
– State of awareness of self & environment
– Responsiveness to external stimulation & inner need
• Unconciousness
– Unawareness of self & environment
– Always w/ diminished responsiveness to external stimuli
• Arousal (level of consciousness)
– Appearance of being awake (displayed by facial muscles,
eye opening, fixity of gaze, body posture)
DISTURBANCES OF LEVEL OF DISTURBANCES OF CONTENT OF
CONSCIOUSNESS CONSCIOUSNESS
• Characterized by: impaired arousal or • Many pathologic conditions impairs
wakefulness w.out altering lvl of consciousness
– Due to acute lesions of ascending – focal brain lesions  isolated
reticular activating system disorders of language or memory
• Most severe degree of depressed – Diffuse, chronic pathologic processes
consciousness = coma  deterioration of mental fx
(dementia) THIS DIFFERS FROM
• Less severe = acute confusional state or
DELIRIUM
delirium Acute confusional Dementia
state
– Pts responds to at least some stimuli
but is sleepy, disoriented, inattentive Lvl of consciousness Impaired Not impaired, except
occasionally late in
In some cases: agitation >> or altered w/ course
drowsiness maybe accompanied by

Course Acute  subacute Chronic, steadily
– autonomic changes: Fluctuating progressive
• Fever, tachycardia, HTN, sweating, Autonomic Often present Absent

hyperactivity
pallor, flushing
– Hallucinations Prognosis Usually reversible Usually irreversbile
– Motor abnormalities
• Tremor, asterixis, myoclonus Distinguishing b/w the 2 syndrome= pivotal step
in evaluating pts w/ altered consciousness
States of Normal & Impaired consciousness
terminologies for describing sates of awareness &
responsiveness of patients
• Normal consciousness
– Awake
– Fully responsive to thought & perception
– Indicates by behavior & speech
– (+) attention to & interaction w/ immediate
surroundings
– May fluctuate to mild general inattentiveness but
latter circumstances can be brought back to state
of full alertness & fx
– Mildest degree:
• Confusion • slight & overlooked
• Roughly oriented time & place,
– Inability to think w/ occasional irrelevant & slowness of
customary speed, thinking
clarity, coherence • Responses inconsistent, attention span
reduced, unable to stay to one topic
– Marked by degree of • Disoriented & easily distractable
inattentiveness & – Severe confused & inattentive
disorientation persons
– Implies degree of • Unable to do more than carry out
imperceptiveness & simplest commands
• Inconsistent & brief in sequence
distractibility
• Speech limited to few words or phrases
“clouding of the • Appearance of unaware
sensorium” • Disoriented in time & place
• Don’t grasp immediate situation
• Miss identify people or objects
• Illusions may lead to fear & agitation
• Degree of confusion Delirium
varies from 1 time of • Observed most often in
day to another alcoholics (not
• Tends to be least exclusively)
pronounced in morning • Vivid hallucinations
• Increases as day wears • Extreme agitation
on • Trembling, startling
• Peaking in early • Convulsion
evening hours • Overactivity of
“sundowning” = pts is
autonomic nervous
fatigued, environmental
system
cues not as clear
• Drowsiness • Stupor
– Inability to sustain wakeful – Patient can be roused only
state w/out application of by vigorous + repeated
external stimuli stimuli
– Mental, speech, physical – Cannot be sustained w/out
activity reduced repeated stimulation
– Pts shift positions naturally; – Responses to spoken
lids droop, snoring, jaw & commands (-) or curtailed
limb muscles slack, limbs or slow & inadequate
relaxed  indistinguishable
– Restless/stereotyped motor
from light sleep
activity common
– Sometimes slow arousal
– When left unstimulated,
elicited by speaking to pts
or apply tactile stimulus pts quickly drift back to
deep sleep-like state
– Eyes move outward upward
Coma
• Pts incapable of being • Sleeping & Coma
aroused by external stimuli or – Sleeping persons may still
inner need respond to stimuli & capale of
• Deepest stage mental activity = dreams
(leaves traces of memory)
– No meaningful or purposeful
• Thus differing from stupor or
reaction of any kind coma
– Corneal, pupillary, pharyngeal – Most important difference:
responses diminished • Person sleep  stimulated  can
• Lighter stage be roused to normal & persistent
consciousness
(semicoma/obtudation)
– Physiologic differences:
– Reflexes can be elicited
• Cerebral O2 uptake doesn’t
– Plantar reflexes flexor/extensor decrease during sleep (does in
(Babinski sign) coma)
Pathophysiology
• Normal consciousness maintained by intact reticular activating
system in brain stem & its central connections to thalamus &
cerebral hemispheres
• RAS keeps awake & alert during waking hrs
• Disorders affecting these areas  disordered arousal,
awareness  altered state of consciousness
• Focal brain lesion below tentorium interfere reticular activating
system  coma
• Focal lesion above tentorium in 1 cerebral hemisphere  coma
only if contralateral side simultaneously involved or
compressed
• Diffuse lesions affects fx of brain as whole includes RAS 
Coma
Glasgow Coma Scale (GCS)
• Scale measuring lvl of consciousness
William Howlett. Neurology in Africa. Available from: http://www.uib.no/filearchive/chapter9_neurology.pdf
Flinders university Clinical Skill Information Sheet

Penurunan Kesadaran
berdasarkan Etiologi
LI 2
Lange. Clinical neurology 7th edition
William Howlett. Neurology in Africa. Available from:
Adams & Victors Principles of Neurology
http://www.uib.no/filearchive/chapter9_neurology.pdf
Penurunan Kesadaran dg etiologi
Extracranial
• Hipoksia
• Hiper/hipoglikemi
• Hiperurisemi
• Hepatic Encephalopathy
• Hiponatremia
Hypoxia – Global ischaemia
• O2 & glucose removed from brain  acute drop in
cerebral blood flow (CBF) to 25 mg/min/100 gr brain
tissue from (N) 55 ml/min/100 gr  slowing of EEG
& syncope/impaired consciousness
• CBF drop <12 -15 ml/min/100 g  electrocerebral
silence, coma, cessation of neuronal metabolic &
synaptic fx
• Lower lvl of ischemia = tolerated if acquired more
slowly (but neuron cannot survive when flow is <8-
10 ml/min/100g ~1/2 (N))

Hypoglycemia
• Most common cause: insulin Clinical findings

overdose in diabetic pts • Tachycardia
• & oral hypoglycemic drugs, • Sweating
alcoholism, malnutrition, hepatic • Pupillary dilateion
failure, insulinoma, insulin-secreting • Followed by confusional state w/ somnolence or
fibroma, sarcoma, fibrosarcoma agitation
• Neurologic ssx dev over minutes-hrs • Progresses in rostral-caudal fashion
• Prolonged hypoglycemia =< 30 • Mimic mass lesion causing transtentorial herniation
mg/dL  irreversible brain damage • Coma ensues + spasticity, extensor plantar
responses
Treatment: • Decorticate & decerebrate posturing
• Dx: blood glucose lvl • Signs of brainstem dysfx subsequently appear
• Th/ w/ glucose 50 mL of 50% – Abnr ocular movements
dextrose IV immediately before BG – Loss pupillary reflexes
lvl known • Respi depression, bradycardia, hypotonia,
• Improvement in lvl of consciousness hyporeflexia  supervene (irreversible brain
= w/in minutes after admn glucose damage imminent)
in pts w/ reversible hypoglycemic • Hypoglycemic coma often associated w/ focal neuro
encephalopathy signs & focal/generalized seizures
https://basicmedicalkey.com/41-3/
Hyperglycemia
• 2 hyperglycemic syndromes
– Diabetic ketoacidosis
• In diabetes  acetone bodies
present in high []
– Hyperosmolar nonketotic
hyperglycemia
Produce encephalopathy or coma
Pathogenesis:
• Impaired cerebral metabolism,
• Intravasc coagulation (hyperviscosity)
• brain edema (due to rapid correction of
hyperglycemia)
– Severity of hyperosmolarity
correlates well w/ depression of
consciousness
– Degree of systemic acidosis
doesn’t
• Clinical findings • Th/ & Prognosis
– Blurred vision – Insulin
– Dry skin – Fluid + electrolyte (esp K+ & P
– Anorexia replacement)
– Polyuria
– AB (concomitant infx)
– Polydipsia
– Death related to sepsis, CVD
• PF:
or cerebrovasc complication
– Hypotension
or renal failure
– Other signs of dehydration (esp
– Hyperosm nonketotic 
in hyperosmolar nonketotic
hyperglycemia) fluid replacement is most
– Deep, rapid (Kussmaul) respi = important
DKA • 0,5 N saline admn except
– Impaired consciousness mild  to pts w/ circulatory
coma collapse  NORMAL
– Focal neuro signs & generalized SALINE
or focal seizures = common in • Insulin also req
hyperosm nonketotic
– Death due to misdx or
hyperglycemia
coexisting disease
HypoNatremia
Clinical findings: • Chronic hypoNa ~110 mEq/L =
• HypoNa+ <Na <120 mEq/L of whatever assx
cause  neuronal dysfx due to • Th/
intracellular movement of water 
neuronal swelling & loss KCl from cells – Immediate management:
• Water restriction
Ssx: Neuro signs: • Infusion of hypertonic saline
• Headache • Confusional or w/out IV furosemide (for
state/coma severe)
• Lethargy • Papilledema – >> rapid correction  central
• Confusion • Tremor pontine myelinolysis (disorder of
• Weakness • Asterixis white matter)  confusional
• Muscle • Rigidity state, paraparesis, quadriparesis,
cramps • Extensor plantar dysartria, dysphagia,
responses hyper/hyporeflexia, extensor
• Nausea &
• Focal or plantar responses
vomiting generalized – Severe – locked in syndrome,
seizures coma, death
HyperCa2+
• Symptoms: • The myopathy spares bulbar muscles

– thirst, polyuria, constipation, nausea and tendon reflexes are usually
and vomiting, normal.
– abdominal pain, anorexia, and flank • Dx confirmed:
pain from nephrolithiasis. – elevated serum calcium level,
• Neurologic symptoms: – sometimes increased parathyroid
– serum calcium levels >17 mg/dL hormone
(8.5 mEq/L) – levels and a shortened QT interval on
– headache weakness, and lethargy. the ECG.
• Physical examination: • Treatment:
– dehydration, abdominal – initially by vigorous intravenous
distention, focal neurologic signs, hydration with 0.45% or 0.9% saline
myopathic weakness, and a – usually requires central venous
confusional state that can pressure monitoring.
progress to coma. • Patients with hypercalcemia should be
– Seizures are rare. evaluated for occult cancer, which
may be the underlying cause.

Hypocalcemia
• Symptoms: • Carpopedal spasm may occur

– irritability, delirium, psychosis spontaneously or following tourniquet-
with hallucinations, depression, induced limb ischemia (Trousseau sign).
nausea and vomiting, abdominal • Cataracts and papilledema are sometimes
pain, and paresthesias of the present, and chorea has been reported.
circumoral region and distal
• Seizures or laryngospasm can be life-
extremities.
threatening.
• The most characteristic • Serum calcium levels <9 mg/dL (4.5
physical signs: overt or mEq/L)
latent tetany. – Ca+ also decreased in hypoalbuminemia
without affecting ionized calcium and
• Neural hyperexcitability:
hypocalcemia with normal ionized calcium
contraction of facial muscles = asymptomatic.
in response to percussion of – The ECG may show a prolonged QT interval.
the facial (VII) nerve • Treatment

anterior to the ear – intravenous calcium gluconate
– seizures, if present, + phenytoin or
(Chvostek sign). phenobarbital.
Encephalopathy
• Term for any diffuse disease of the brain that alters brain fx &
structure
• May be caused by:
– infectious agents, metabolic, or mitochondrial dsyfx, brain tumor or
increase pressure in skull, prolonged exposure to toxic elements,
chronic progressive trauma, poor nutrition, lack O2 or BF to brain
• Hallmark = altered mental state
• Depending on type & severity; common neuro ssx:
– Progressive loss of memory & cognitive ability
– Subtle personality changes, inability to concentrate
– Lethargy & progressive loss of consciousness
– Other neuro ssx: myoclonus, nystagmus, tremor, muscle atrophy
+ weakness, dementia, seizures, loss ability to swallow or speak
Encephalopathy. American College of Physicians. https://www.mnhospitals.org/Portals/0/Documents/patientsafety/Delirium/ACP%20Encephalopathy

%20Coding%20Article.pdf
Categories of encephalopathy
Acute Chronic
• Acute/subacute global, fxal alteration • Chronic mental status alteration:
of mental status due to systemic slowly progressive
factors
• Result from permanent,
• Reversible when abnr corrected,
irreversible, structural changes
return to baseline mental status
w/in brain itself
• Further identified:
– Toxic • Examples:
• Medications, drugs, chemicals – Anoxic brain injury
– Metabolic – Chronic traumatic encephalopathy
• Metabolic disturbances – Heavy metals
– Toxic-metabolic – HIV-related
• Causes: acute organ failure (hepatic & – Hereditary enz def
renal; alcohol; dehydration; – etc
electrolyte imbalace; fever; HTN; Acute intra-cranial processes
hypoxemia; drugs; infx (sepsis); (stroke/traumatic lesions) should not be
meds; toxic chem; Wernicke classified as acute encephalopathy but
(thiamine def) considered as alteration of consciousness or
concussion
Encephalopathy. American College of Physicians. https://www.mnhospitals.org/Portals/0/Documents/patientsafety/Delirium/ACP%20Encephalopathy
%20Coding%20Article.pdf
Hepatic Encephalopathy
Liver disease
Hepatic coma  elevation of
blood NH3 to 5-6 x (N)  coma impair hepatocellular detoxifying mechanism or
portosystemic shunting of venous blood
• As complication of cirrhosis,
portosystemic shunting, ammonia & toxins accumulate in blood
chronic active hepatitis, or
fulminant hepatic necrosis diffuse to brain
(following viral hepatitis)
• Alcoholism = most common cerebral ssx
underlying disorder
Cilinical findings:
• Syndrome may be chronic • Ssx of encephalopathy may precede
progressive or acute (onset) systemic ssx: nausea, anorexia, weight
• Latter case  GI hemorrhage loss
(freq precipitating cause) • Recent GI bleeding, consume high-prot
foods, use of sedatives or diuretics,
systemic infx = clue to cause of clinical
decompensation
• PF:
– Systemic signs of liver disease • Treatment
– Cognitive disturbances: somnolence, – Restrict dietary proteins
agitation, coma – Reverse electrolyte disturbances
– Occular reflex usually brisk & hyperglycemia
– Nystagmus; tonic downward ocular deviation – Discont.drugs causing
& disconjugate eye movement seen decompensation
– Most helpful neuro sign of metabolic – AB, Frozen fresh plasma or vit K
disturbance (not restricted to liver) = – Oral/rectal + lactulose 20-30 g 3-
ASTERIXIS (flapping tremor of outstretched 4x/d decreases colonic pH
dorsiflexed hands or feet from impaired ammoia abs.
postural control) – Neomycin 1-3g PO 4x/d reduce
– Other: seizures, tremors, spasticity, rigidity, ammonia forming bacteria in
posturing colon
• Lab – Benzodiazepine rec antagonist
– Bilirubin, transaminase, ammonia, PT/PTT, flumazenil
respi alkalosis – Orthotopic liver transplant req
– Most specific CSF abnormalitis = elevated some cases
glutamine – Prognosis: correlates w/ severity
– EEF: diffuse slow triphasic waves of hepatocellular >> neuro dysfx

Hypertensive Encephalopathy
• Sudden increase in BP (+/- preexisting chronic HTN) 
encephalopathy & headache (dev over period of sev hrs to days
• Vomiting, visual disturbances, focal neurologic deficits, focal or
generalized seizures can occur
• BP >250/150 mmHg usually req to precipitate the syndr in pts
w/ chronic HTN
• Prev normotensive pts may be affected at lower pressures
• Coexisting renal failure increase risk of HE
• Cerebrovasc spam, impaired autoregulation of cerebral BF,
intravasc coagulation = proposed as cause of neurossx
• small infacts & petechial hemorrhage  affect brainstem most
prominently + other subcortical gray & white matter regions

• Prevention
• Clinical findings
– Early th/ of uncomplicated
– Most useful confirming HTN & prompt recognition
dx: ophthalmoscopy of elevated BP (e.g acute
• Retinal arteriolar spasm glomerulonephritis,
• Papilledema, retinal eclampsia)
hemorrhage, exudates • Treatment
(+) – Lowering BP  rapid
– Lumbar puncture = resolution of ssx
normal or elevated CSF – Na nitroprusside (release
pressure & prots vasodilator, NO) IV cont
infusion initial rate 0,5
mg/kg/min  increased to
3-10 mg/kg/min required

Renal - Uremia
• EEG
• Uremia  accumulation of
– Slow triphasic or parozysmal
dialzyable small molecular toxins
spikes or sharp waves
(phenolic derivatives of Aromatic
AA) • Acute management:
• Renal failure (esp acute onset or – Hydration
rapid progressive)  – Protein
encephalopathy or coma + – Salt restriction
hyperventilation & prominent • Long-term management:
motor manifestation – Reverse cause (e.g urinary tract
– Tremor, asterixis, myoclonus, obstruction)
tetany – Dialysis, kidney transplant
• Lab: • Dialysis itself can produce
– Abnr elevated serum urea encephalopathy (dialysis
nitrogen, creatinine, K+,
disequilibrium syndrome)
met.acidosis
result from hypoosmolarity
– Use briefer period of dialysis at
reduced rate of BF
Pulmonary encephalopathy
• Impairment of • Exam: papilledema,
consciousness + pulmo asterixis, myoclonus,
insufficiency  hypercapnia confusional state or coma
• Pts w/ lung disease or • Tendon reflexes decreased,
brainstem or neuro pyramidal signs may
disorders affect respi fx  present
encephalopathy related to – plantar extension and
hypoventilation hyperreflexia
• SSx: • Seizure occasional
– Headache, confusion, • ABG = respi acidosis
somnolence • Th/ ventilatory support to
decrease hypercapnia to
maintain adeq oxygenation
Wernicke Encephalopathy
• Complication of chronic alcoholism • Clinical findings

• Occurs in other disorders assc w/ – TRIAD: OPHTHALMOPLEGIA, ATAXIA,
malnutrition CONFUSIONAL STATE
• Caused by def of thiamin (B1) – Most common ocular abnr: nystagmus,
• Pathologic features: abducens (VI) nerve palsy, horizontal-
– Neuronal loss vertical gaze palsy
– Demyelination – Ataxia gait
– Gliosis in periventricular gray – Global confusion + prominent disorder
matter of immediate recall & recent memory
– Prolif of small BV & petechial – Absent ankle jerks
hemorrhages may be seen – Ypothermia & hypotension may occur
• Areas most commonly involved: do to hypothalamic involvement
– Medial thalamus, mammilary – Pupillary abnr: mild anisocoria, sluggish
bodies, periaqueductal gray reaction to light
matter, cerebellar vermis, – Periph blood smear: macrocytic anemia
oculomotor, abducens, vestibular – MRI: atrophy of mammillary bodies
nuclei
• Treatment • Prognosis
– Prompt adm of thiamine – + th/  ocular abnr
– Initial dose 100 mg IV begin to improve w/in 1
(before or +dextrose) day & ataxia & confusion
avoid precipitating or w/in 1 week
exacerbating disorder – Ophthalmoplegia,
– Parenteral thiamine vertical nystagmus,
cont.for sev days acute confusion
– Maintenance req for reversible w/in 1 mo
thiamine ~1mg/d (throu – Major long term
diet) although abs compliation = Korsakoff
impaired in alcoholics syndrome (amnestic
syndr)

Penurunan Kesadaran dg etiologi
Intracranial
• Trauma
• CVD (stroke iskemik/hemoragik)
• Infeksi (meningitis, encephalitis)
• Intoksikasi
• Peningkatan tekanan intrakranial (TIK)
• Tumor intracranial
• Encephalopathy
• Mati batang otak
• Coma
Diffuse Encephalopathies/metabolic coma
• Hypoglycemia and drug intoxication • Asterixis, myoclonus, and tremor
• other processes that affect the brain preceding coma = important clues that
suggest metabolic disease.
diffusely:
• Symmetric decorticate or decerebrate
– meningitis, subarachnoid hemorrhage,
posturing can be seen with hepatic,
and seizures.
uremic, anoxic, hypoglycemic, or sedative-
• The clinical presentation is distinct drug–induced coma.
from that of a mass lesion. • Reactive pupils in the presence of
• There are usually no focal signs: otherwise impaired brainstem function is
– hemiparesis, hemisensory loss, or the hallmark of metabolic encephalopathy
aphasia • The few metabolic causes of coma that
– no sudden loss of consciousness also impair pupillary reflexes:
• Except in some cases of subarachnoid – massive barbiturate overdose with
hemorrhage apnea and hypotension,
• History reveals a period of progressive – acute anoxia,
somnolence or toxic delirium followed – marked hypothermia,
by gradual descent into a stuporous – anticholinergic poisoning (large pupils)
and finally comatose state – opioid overdose (pinpoint pupils).

Metabolic encephalopathy (+ widespread
anatomic damage to hemispheres)
• BF may stay near normal
• Metabolism greatly reduced
• Coma arises from seizures (met & BF greatly
increase)
• Extremes of body temperature >410C or below
300C also induce coma through nonspecific
effect on met activity of neurons

SEIZURES
• Sudden & >> neuronal discharge  epileptic seizure
 coma
• Focal seizure activity = little effect on consciousness
 spread 1 side to another  extension of seizure
discharge  deep central neuronal structures 
paralyze their fx
• In seizures in which consciousness interrupted from
very beginning = diencephalic origin postulated

Close head injury
concussive
Enormouse vibration abrupt
transmitted head injury
increase in set up in paralysis of
to brain (commotio
ICP skull nervous fx
cerebri)
• Sudden swirling motion of brain induced by

acceleration/decceleration from blow to head
 rotation (torque) or cerebral hemisphere
around axis of upper brainstem

Head Trauma
• Blunt head trauma  confusional state/coma
Acceleration or
decceleration forces shearing of white
& physical matter
deformation of skull
torn BV, vasomotor contusion from contact

changes, brain b/w inner surface of skull
edema, increased & polar regions of
ICP cerebral hemispheres

Concussion
• Transient loss of consciousness for secs - minutes w/out
demonstrable structural defects
• Unconsciousness assc w/ normal pupillary & ocular reflexes,
flaccidity & extensor plantar responses
• Return of consciousness followed by confusional state lasts
from minutes  hrs
• Characterized by: prominent retrograde & anterograde
amnesia
• Headache, dizziness or mild cognitive impairment may persist
for wks
• Unconsciousness prolonged  delayed in onset after an
evident interval or assc w/ focal neurologic abnr,
posttraumatic intracranial hemorrhage considered

Intracranial hemorrhage
• Epidural hematoma
– Results from lateral skull fracture lacerates middle meningeal artery
or vein
– Pts +/- lose consciousness initially  lasting sev hrs – 1-2 days  rapid
evolution; over hrs of headache, progressive obtundation, hemiparesis
 ipsilateral pupil dilation from uncal/brain herniation  Death
follow if th/ delayed
• Subdural hematoma
– Acute, subacute, chronic
– Time b/w trauma & onset of ssx typically longer
– Hemorrhage located over cerebral convexities, assc skull fractures
uncommon
– Hematoma in posterior fossa uncommon
• Intracerebral contusion (bruising) or hemorrhage

ACUTE & CHRONIC TRAUMATIC ENCEPHALOPATHIES
Beta-amyloid comes from a
larger protein found in the
fatty membrane
surrounding nerve cells.
Beta-amyloid is chemically
"sticky" and gradually builds
up into plaques.
Abbreviations: APOE, apolipoprotein E; PTSD, post-traumatic stress disorder; TBI, traumatic brain injury.
Spectrum of pathological features and outcomes of mild and severe TBI. Acute and chronic traumatic encephalopathies:
pathogenesis and biomarkers.http://www.nature.com/nrneurol/journal/v9/n4/fig_tab/nrneurol.2013.36_F1.html
Stroke
• Rapidly developing clinical signs of focal (or
global) disturbances of cerebral fx, + ssx
lasting 24 hrs or longer or leading to death w/
no apparent cause other than vascular origin
• TIA = <24 hrs & pts w/ stroke ssx caused by
subdural hemorrhage, tumors, poisoning,
trauma excluded
• Types of stroke: ISCHEMIC & HEMORRHAGIC
The global burden of cerebrovascular disease. Thomas Truelsen. WHO

Ischemic stroke (infarction)
• Atherosclerotic or embolism obstruction of large cervical &
cerebral arteries  Thrombotic cerebral infarction 
ischemia in all or part of teritorry of occluded artery
– This can also be due to more distal cerebral arteries
• Embolic cerebral infarct = due to embolism of clot in
cerebral arteries coming from other parts of arterial system,
e.g. cardiac lesions, or rhythm disturbances w/ stasis of blood,
allows clotting w/in heart (as seen in atrial fibrillation)
• Lacunar cerebral infarction = small deep infarcts in
territory of small penetrating arteries due to local disease of
these vessels mainly related to chronic HTN

Hemorrhagic stroke
• Spontaneous intracerebral hemorrhage (as
opposed to traumatic) = mainly due to
arteriolar HTN disease, rare: coagulation
disorder, vasc malformation w/in brain, diet
(high alcohol consumption, low blood chol [],
high BP, etc)
• Cortical amyloid angiopathy (consequence of
HTN) caused of cortical hemorrhage esp in
elderly
Subarachnoid hemorrhage
• Group of strokes mainly due to rupture of
aneurysm at bifurcations of large arteries at
inferior surface of brain
• Oftern don’t cause direct damage to brain
• Dev ssx in accordance to stroke definitions

RF of cerebrovasc disease
• Inherent biological traits: age, sex,
physiological characteristics  high BP, serum
chol, fibrinogen, behaviors: diet, alcohol,
physical inactivity, soacial char (temperature,
altitude), geographical, psychosocial
• Previous TIA or stroke, ischemic heart disease,
atrial fib, glucose intolerance, all increase risk
of stroke

Raised ICP
• Common neurologic
complication
• Increased in brain vol,
cerebral BF, CSF vol
• ICP normal values =
• <10 – 15 mmHg (adults);
& older children;
• 3-7 mmHg young
children
• 1.5 – 6 mmHg term
infants
• ICP >20-25 mmHg  th/
• Sustained >40 mmHg ICP =
Severe, life-threatening IC
HTN
Management of Raised Intracranial Pressure. Indian J Pediatr (2010) 77:1409–1416. http://medind.nic.in/icb/t10/i12/icbt10i12p1409.pdf

https://basicmedicalkey.com/neurologic-disorders/
https://evidencebasedpractice.osumc.edu/Doc
uments/Guidelines/ICP%20algorithm.pdf
Intracranial Mass
Brain abscess
• uncommon disorder, 2% of intracranial masses.
• Common conditions predisposing to brain abscess, in
approximate order of frequency, are:
– blood-borne metastasis from distant systemic (especially pulmonary)
infection;
– direct extension from parameningeal sites (otitis, cranial osteomyelitis,
sinusitis);
– an unknown source;
– infection associated with recent or remote head trauma or
craniotomy;
– infection associated with cyanotic congenital heart disease.

• Most common pathogenic • The course is that of an
agents: aerobic, anaerobic, expanding mass lesion, and its
and microaerophilic usual presentation is with
streptococci, and headache and focal signs in a
conscious patient.
gramnegative anaerobes:
bacteroides, fusobacterium, • Coma may develop over days
but rarely over hours.
and prevotella.
• Staphylococcus aureus,
Proteus, and other gram-
negative bacilli are less
common.
• Actinomyces, Nocardia, and
Candida are also found.
• Multiple organisms are
present in the majority.

The diagnosis is strongly • CSF cultures are usually
supported:
negative.
• avascular mass on angiography
or a lesion with a contrast- • Marked clinical
enhanced rim on CT scan or deterioration may
MRI. follow lumbar puncture
Examination of the CSF:
in patients with brain
• an opening pressure >200 mm
water in 75% of patients;
abscess and so lumbar
• pleocytosis of 25–500 or more puncture should not be
white cells/mm3, depending performed if brain
on the proximity of the abscess is suspected.
abscess to the ventricular
surface and its degree of
encapsulation; Opening pressure: The pressure
of the cerebrospinal fluid that is
• elevation of protein (45–500 detected just after a needle is
mg/dL) ~60% of patients. placed into the spinal canal. It is
normally 100 to 180 mm H20.
Lange. Clinical neurology 7th edition Medical Dictionary, © 2009 Farlex and Partners
• Treatment of pyogenic brain • If the causal organism is
abscess = antibiotics alone or + unknown, broad coverage with
surgical drainage. antibiotics is indicated.
• Surgical therapy strongly • If staphylococcal infection is
suspected, + oxacillin or nafcillin
considered when there is a
3 g intravenously every 6 hours.
significant mass effect or the
• methicillin-resistant staph is now
abscess is near the ventricular
so common, many centers begin
surface with vancomycin 1 g every 12
– catastrophic rupture into the hours adjusted to serum levels.
ventricular system may • To cover staphylococci and
occur aerobic gram-negative bacilli
• Medical treatment alone is (trauma patients), nafcillin +
indicated for: cefotaxime or ceftriaxone is
recommended.
– surgically inaccessible,
multiple, or early abscesses.

• Glucocorticoids may
attenuate edema
surrounding the
abscess.
– Response to medical
treatment is
assessed by the
clinical examination
and by frequent CT
scans or MRIs.
• When medically
treated patients do
not improve 
needle aspiration of
the abscess is
indicated to identify
the organisms
present.

Brain Tumor
• Primary or metastatic tumor • Brain tumor is suspected  CT scan or
of CNS rarely present w/ MRI should be obtained.
• Biopsy may be required.
coma  do so when
hemorrhage into tumor or • Chest x-ray is useful; lung carcinoma is
the most common source of intracranial
tumor induced seizures metastasis and because other tumors
occur that metastasize to the brain commonly
• Most often coma occurs late involve the lungs first.
in clinical course of brain
TREATMENT
tumor • corticosteroid th/ is often remarkably
– (+) hx of headache effective in reducing tumor-associated
– Focal neurologic deficits vasogenic brain edema (leaking
– Altered consciousness capillaries) and improving related
– Papilledema presenting sign neurologic deficits.
in 25% cases • Specific approaches: excision,
radiotherapy, and chemotherapy,
depending on the site and nature of
the lesion
Herniation
• Dislocation of portion of
cerebral or cerebellar
hemisphere from (N) position
 adjacent compartment
bounded by dural folds
• Herniation = transfalcine
(across falx) or transtentorial
(through tentorial aperture) or
named by structure displaced:
cerebellar, uncal, etc

Large, destructive, space consuming lesions
Brain displacement &
of cerebrum: hemorrhage, tumor, abscess,
infarct + brain swelling
Herniations
Consequence of lateral
displacement
Indirectly lateral & downward displacement

of subthalamic-upper brainstem structure & upper midbrain (particularly
herniation of medial part of temporal lobe cerebral peduncle) pushed against
(uncus, hippocampus) opposite free edge of tentorium
creasing of lateral edge of

peduncle called Kernohan notch or
Kernohan-Woltman phenomenon)
opening in tentorium
weakness & Babinski sign ipsilateral

to hemispheral lesion
impair consciousness
extensor posturing on that side
Ipsilateral posterior cerebral • Infarcts & hemorrhage
artery of ipsilateral
oculomotor nerve may also be don’t usually cause coma
compressed at edge of  create mass effect  20
tentorium compresses upper
brainstem
– Exceptions: massive strokes
affecting territory of internal
infarct of ipsilateral occipital carotid artery  drowsy &
lobe in former inattentive from onset (even
before brain swelling)
• Most often simply apathetic
+ tendency to keep their
eyes closed 
opthalmoparesis + pupillary misinterpreted as tumor
enlargement

Management of Raised Intracranial Pressure. Indian J Pediatr (2010) 77:1409–1416. http://medind.nic.in/icb/t10/i12/icbt10i12p1409.pdf
Intoxication
Drugs
• General anesthetics
• Alcohol
• Opiates
• Barbiturates
• Phenytoin
• Antidepressants
• Benzodiazepines
Induce coma by direct effects on neuronal membranes in cerebrum &
RAS or on neurotransmitters & their receptors
Others:
• Methylalcohol & ethylene glycol = both acts directly & produce
metabolic acidosis

Ethanol intoxication
• Confusional state w/ nystagmus, dysarthria, limb, gait ataxia
• Non-alcoholics = correlates w/ blood ethanol levels
• Chronic-alcoholics; dev tolerance to ethanol = high levels w/out appearing
intoxicared
• Lab studies to confirm dx
– Blood alcohol lvls
– Serum osmolality
• >> calculated osmolality (2x serum Na + 1/20 serum glucose + 1/3 serum urea
nitrogen) by 22 mosm/L for every 100 mg/dL ethanol present
• Intoxicated pts (high risk for head trauma)
• Alcohol ingestion  life threatening hypoglycemia
• Chronic alcoholism  increase risk of bacterial meningitis
• Th/ not req unless withdrawal syndrome
• Alcoholics should (+) thiamine = prevent Wernicke encephalopathy

Ethanol Withdrawal
• 3 common withdrawal syndromes recognized

Tremulousness & Seizures Delirium tremens
hallucination • Occur w/in 48 hrs post• Most serious syndrome begins 3-5 days
• Self limited (w/in 2 after cessation
abstinence (~7-24 hrs)
days after cessation of • Lasts for upto 72 hrs
• Anticonvulsants not •
drinks) Characterized by:
usually req  ceases
– Confusion
• Tremolous, agitation, spontaneously
– Agitation
anorex, insomnia, • Unusual features:
tachycardia, HTN – Fever
– >6 seizures – Sweating
• Confusion mild
– Status epilepticus – Tachycardia
• Illusions &
– Prolonged – HTN
hallucinations (visual)
– Hallucinations
25% pts postictal state
• Death = concomitant infx, pancreatitis,
• Th/+ diazepam 5-20 • PROMPT SEARCH FOR CVD collapse, trauma
mg or OTHER CAUSES (e.g: • Th/: diazepam 10-20 mg IV (repeat every 5
chlordiazepoxide 25- head trauma/infx) minutes)  pts is calm
50 mg oral every 4 hrs • Observe pts for 6-12 hrs
• Correction of fluid & electrolyte abnr &
 terminate syndr, • Diazepam or hypoglycemia
prevent more serious chlordiazepoxide • Total req for diazepam may >100 mg/h
sequences of sometimes given • Comcomitanat B-adrenergic receptor
withdrawal prophylactically blockade (atenolol) 50-100 mg/d
recomended

Sedative Drug Intoxication
• Classic sign:
– Confusional state/coma
– Respi depression
– Hypotension
– Hypothermia
– Reactive pupils
– Nystagmus or absence of ocular movements
– Ataxia
– Dysarthria
– Hyporeflexia
• Most commonly: benzodiazepines & barbiturates
• Glutethimid or very high doses barbiturates  large fixed pupils
• Decerebrate & decorticate posturing
• Dx: toxicology analysis of blood, urine, gastric aspirate
• Management: support respi & circulatory fx while drug being cleared
Sedative drug withdrawal
• Intake stopped abruptly
• Freq & severity depend upon duration of drug intake & dose
& T ½ of drug
• Most often in pts taking large doses of at least sev wks
• Intermediate/short-acting agents = most likely produce
withdrawal symptoms
• Commonly dev 1-3 days after cessation of short-acting agents
• Ssx identical to ethanol withdrawal & similar self-limited
• Myoclonus seizures may appear 3-8 days after  may req
treatment
• Th/: long-acting barbiturate (phenobarbital, orally: maintain
calm state w/out sign of intoxication  tapered over ~2 wks)

Examination
Opioid • Cardinal features of opioid overdose

– pinpoint pupils, constrict in
bright light
• Opioids – respiratory depression
– produce analgesia, mood changes, • These features can also result from
confusional states, coma, pontine hemorrhage, distinguished
respiratory depression, pulmonary by response to opioid antagonist
edema, nausea and vomiting, naloxone.
pupillary constriction, hypotension, • + naloxone  pupillary dilation + full
urinary retention, reduced GI recovery of consciousness occur
motility. promptly.
Treatment
• Chronic use = tolerance and
• IV naloxone, 0.4–0.8 mg, sometimes
physical dependence. ventilatory support.
– naloxone’s action may be as short as
1 hour—and many opioids are
longer-acting—it should be
readministered as the patient’s
condition dictates.

Anticholinergic Drugs
• Muscarinic anticholinergic drugs are used to treat gastrointestinal
disturbances, parkinsonism, motion sickness, and insomnia.
• Antipsychotic drugs, tricyclic antidepressants, and many antihistamines
also exhibit prominent anticholinergic activity.
• Overdose with any of these agents  confusional state with agitation,
hallucinations, fixed and dilated pupils, blurred vision, dry skin and
mucous membranes, flushing, fever, urinary retention, and tachycardia.
• In some cases, the diagnosis can be confirmed by toxicologic analysis of
blood or urine.
• Symptoms usually resolve spontaneously,
– Treatment may be required, especially if life-threatening cardiac arrhythmias
occur.
– cholinesterase inhibitor physostigmine  interfering with the breakdown of
acetylcholine  reverse abnr
– Physostigmine  bradycardia and seizures, rarely used.

Phencyclidine
• Phencyclidine (PCP) produce drowsiness, agitation, disorientation,
amnesia, hallucinations, paranoia, and violent behavior.
• Neurologic examination:
– large or small pupils,
– horizontal and vertical nystagmus,
– ataxia, hypertonicity, hyperreflexia, and myoclonus.
• Severe  complication  hypertension, malignant hyperthermia, status
epilepticus, coma, and death.
• Benzodiazepines may be useful for sedation and treating muscle spasms,
and antihypertensives, anticonvulsants, and dantrolene (for malignant
hyperthermia) may be required.
• Symptoms and signs usually resolve within 24 hours

Meningitis
BACTERIAL MENINGITIS
• Leading cause of acute confusional state
• Early dx  improves outcome
• Predisposing condition:
– Systemic (esp respiratory) or parameningeal infx
– Head trauma
– Anatomic meningeal defects
– Prior neurosurgery
– Cancer
– Alcoholism
– Immunodef states
• Etiologic organisms varies w/ age & predisposing conditions
Clinical Neurology. Lange. 7th edition

Bacteria typically Pathophysiology of Bacterial Meningitis
gain access to the
CNS Polysaccharide
1. local tissue bacteria capsules,
• colonizing the mucous invasion, lipopolysaccharides,
membranes of the
2. bacteremia, outer membrane
nasopharynx
3. hematogenous proteins contribute
• Spread to the meninges
seeding of the to the bacterial
directly, through invasion and
anatomic defects in the subarachnoid space.
virulence.
skull
• from parameningeal
sites: the paranasal
sinuses or middle ear
promote blood–
brain barrier
permeability, low levels of
Inflammatory
vasogenic cerebral antibody and
response: release of
edema, complement present
inflammatory
in the subarachnoid
changes in cerebral cytokines, IL 1, 6 and
space inadequate to
blood flow, TNF α
contain the infection.
and perhaps direct
neuronal
Clinical Neurology. Lange. toxicity
7th edition
https://clinicalgate.com/infections-of-the-central-nervous-system/
S&S
• At presentation, most • Physical examination:
patients have had – Fever
symptoms of meningitis – signs of systemic or
for 1–7 days parameningeal infection,
– fever, such as skin abscess or
– confusion, otitis.
– vomiting, – A petechial rash is seen
– Headache, in 50–60% of patients
– neck stiffness, with N. meningitidis
but the full syndrome is
meningitis.
often not present.

• Signs of meningeal
irritation (~80% of cases)
• Often absent in the very
young and very old, or • The level of
with profoundly impaired consciousness, when
consciousness. altered, ranges from
• These signs include: mild confusion to coma.
– neck stiffness on passive • Focal neurologic signs,
flexion, seizures, and cranial
– thigh flexion upon flexion
nerve palsies may occur
of the neck
– resistance to passive
extension of the knee with
the hip flexed (Kernig sign)

MENINGEAL SIGNS
• The Kernig sign is performed
– patient lying supine and the hip and
knee flexed to 90 degrees.
– (+): extension of the knee from this
position elicits resistance or pain in the
lower back or posterior thigh.
• The classic Brudzinski sign https://clinicalgate.com/infections-of-the-central-nervous-system/
– spontaneous flexion of the knees and
hips during attempted passive flexion
of the neck.
• Nuchal rigidity or neck stiffness
– placing the examiner's hand under the
patient's head and gently trying to flex
the neck.
– Undue resistance implies diffuse
irritation of the cervical nerve roots
from meningeal inflammation.
http://www.slremeducation.org/wp-content/uploads/2015/06/Chapter-171.-Meningitis-Encephalitis-and-Brain-Abscess.pdf
http://pdf.yassermetwally.com/ex.pdf
Atypical presentations of ABM occur in infants, older
adults, and immunocompromised patients.
• Infants with bacterial meningitis:
– Fever or hypothermia
– hypoglycemia, poor feeding
– seizures, or irritability (excessive or abnormal crying).
• Examinations:
– findings of jaundice, ill appearance,
– a bulging fontanelle,
– meningeal irritation (including neck stiffness, the Kernig
sign, and the Brudzinski sign)
– fever higher than 40° C
– increased general body tone
predict bacterial meningitis.
• Older and immunocompromised patients:
– higher rate of misdiagnosis that contributes to an
increase in the morbidity and mortality following
an episode of acute meningitis.
– lower proportion of fever, headache, and nausea
or vomiting
– Neck stiffness has a lower sensitivity and
specificity for meningitis in older patients.
– Finally, these populations may present to the
emergency department (ED) with altered mental
status and/or altered level of consciousness but
without a fever.
Lab findings
• Peripheral blood may • Images of the chest,
reveal PMN leukocytosis sinuses, or mastoid
from systemic infection bones may indicate a
or leukopenia due to primary site of
immunosuppression. infection.
• Causative organism can • A brain CT or MRI scan
be cultured from the may show contrast
blood in 40–90% of enhancement
meningitis

• Essential test in all cases of suspected meningitis = prompt
lumbar puncture & CSF examination.
• Gram-stained smears of CSF identify the causative organism in

70–80% of cases.
Prevention
• Children should be routinely immunized against H. influenzae
by vaccination.
• A vaccine is also available for some strains of N. meningitidis
and is recommended for military recruits, college students,
and travelers to areas of ongoing epidemics.
• The risk of contracting H. influenzae or N. meningitidis
meningitis can be reduced in household & other close
contacts of affected patients
prophylactic administration of rifampin, 20 mg/kg/d orally,
– single daily dose for 4 days (H. influenzae)
– two divided doses for 2 days (N. meningitidis).

• Complications of bacterial Complication & prognosis
meningitis:
– headache, seizures,
– hydrocephalus, • Morbidity and mortality from
– syndrome of inappropriate secretion bacterial meningitis are high.
of antidiuretic hormone (SIADH) • Fatalities occur in ~20% of
• A CT scan will confirm suspected affected adults, more often with
hydrocephalus and fluid and electrolyte
status should be carefully monitored to
some pathogens (e.g., S.
detect SIADH. pneumoniae, gram-negative
– residual neurologic deficits (including bacilli) >> others (e.g., H.
cognitive disturbances and cranial— influenzae, N. meningitidis).
especially VIII—nerve abnormalities), • Factors that worsen prognosis
– death include:
– N. meningitidis infections may be – extremes of age,
complicated by adrenal hemorrhage  – delay in diagnosis and treatment,
hypotension  death (Waterhouse– – complicating illness,
Friderichsen syndrome). – stupor or coma, seizures, and
focal neurologic signs.

Tuberculous meningitis
Pathogenesis & pathology
• Considered in pts who • Reactivation of latent infx w/
present w/ confusional M.tuberculosis
state esp (+) hx of Primary infx: inhaling bacillus
pulmonary TB, alcoholism, containing droplets
corticosteroid th/, HIV infx, metastatic dissemination of

others w/ impaired immune blood-borne bacilli from
lungs
responses
• Considered in pts from meninges & surface of brain
areas (Asia, Africa) or

groups (homeless, innercity Organisms remain dormant in
tubercles
drug users) w/ high
incidence TB rupture to subarachnoid
space at later time
TB meningitis
• Main finding: • S&S
– Usually (+) <4 wks at time of
– Basal meningeal exudate presentation:
contain primary MN cells • Fever
• Lethargy
– Tubercles seen on • Confusion
meninges & surface of • Headache
brain – Weight loss
– Ventricles may be – Vomiting
– Neck stiffnes
enlarged as result of – Visual impairment
hydrocephalus – Diplopia
– Surface show ependymal – Focal weakness
exudate or granular – Seizures
• Complications:
ependymitis – Spinal subarachnoid block
– Arteritis result in cerebral – Hydrocephalus
– Brain edema
infarct – CN palsies
– Basal inflammation & – Stroke by vasculitis or compression of BV at
base of brain
fibrosis  compress CN
Treatment
• Started ASAP
• Don’t withheld while waiting for
culture results
• Decision to treat based on CSF
findings
• Lymphocytic pleocytosis &
decreased glucose = suggestive
even when Acid fast bacili smear (-)
PROGNOSIS
• Even + appropriate th/; ~1/3 pts w/
TB meningitis succumb
• Coma at time of presentation =
poor prognosis predictor

Syphilitic Meningitis
• Acute or subacute • ¼ pts w/ T.pallidum infx
usually occur w/in 2 yrs • Treponemes  CNS 
after primary syphilitic meningitis (assx
infx neurosyphilis)  assx
• Most common in young invasion of CNS (assc w/
adults (men > women) CSF pleocytosis,
• Require prompt th/ to elevated prot +ve
prevent irreversible serologic test)
manif of tertiary
neurosyphilis

• S&S – Protein electrophoretograms of CSF =
– Headache, nausea, vomiting, stiff neck, discrete gama-globulin bands
mental disturbances, focal weakness, (oligoclonal bands) not visible in
seizure, deafness, visual impairment have normal CSF
been present for up to 2 mo during
presentation
• Th/
– PF: – Acute SM usually self limited w/ no
•
or minimal sequale
Meningeal irritation
• Confusion or delirium – Advanced manif of neurosyphilis
• Papilledema (vascular & parenchymatous disease:
• Hemiparesis tabes dorsalis, general paresis, optic
• Aphasia neuritis, myelitis) prevented by adeq
th/ of early infx
– CN most commonly affected (in order)
• VII, VIII, III, V, VI, II
– Aqueous penicillin G 2-4x106 U IV
every 4 hrs for 10 days
– Fever typically absent
– Penicillin alergic pts:
tetracyclin/erythromycin 500 mg oral
every 6 hrs 20 days
• Lab findings
– Examine CSF every 6 mo until findings
– CSF findings
are (N)
– Pleocytosis = lymphocytic or MN in character
– Anouther course th/ must be givein if
+ white cell counts ~100-1000/mL
CSF cell count or prot remains
– Protein = mildly or moderately elevated elevated
<200 mg/dL & glucose mildly decreased
– VDRL & serum FTA or MHA-TP test usually
+ve
Lange. Clinical neurology 7 edition
th
Aseptic
meningitis
• Aseptic meningitis refers
to a disorder in which
patients have clinical
and laboratory evidence
of meningeal irritation
with negative results of
routine bacterial
cultures
Viral Meningitis & Encephalitis
• Viral infections of the • Viral meningitis most
meninges (meningitis) often caused by enteric
• Brain parenchyma viruses
(encephalitis) • Viral encephalitis by
• Often present as acute childhood exanthems,
confusional states. arthropod borne
• Children and young agents, HSV 1
adults are frequently
affected.

Pathophysiology
Viral infections can affect

the CNS in three ways:
Hematogenous
neuronal spread of the autoimmune
dissemination of a
virus by axonal transport postinfectious
systemic viral infection
(e.g., herpes simplex, demyelination (e.g.,
(e.g., arthropod-borne
rabies); varicella, influenza).
viruses);

Clinical Findings
Systemic viral infection may cause:

Clinical manifestations:
• skin rash, pharyngitis, lymphadenopathy,
• fever, headache, neck stiffness, pleuritis, carditis, jaundice,
photophobia, pain with eye organomegaly, diarrhea, or orchitis
movement, and mild impairment of • these findings may suggest a particular
consciousness. etiologic agent.
• Patients usually do not appear as ill
as those with bacterial meningitis.
Because viral encephalitis

When signs of meningeal
involves the brain directly
irritation and brain
 marked alterations of
dysfunction coexist, the
consciousness, seizures,
condition is termed
and focal neurologic signs
meningoencephalitis.
can occur.
Lab findings
• CSF analysis MOST IMPORTANT
• Pressure(N) or increased
• Lymphocytic or monocytic pleocytosis present
• Cell counts usually <1000/mL (higher counts in lymphocutic choriomeningitis or
HSV encephalitis)
• PMN pleocytosis can occur
• RBCs can be seen w/ HSV encephalitis
• Protein (N) or slight increased (~80-200 mg/dL)
• Glucose (N) but may be decreased in mumps, HZV, HSV encephalitis
• Gram stains & bacterial, fungal, acid fast bacillus cultures (-)
• Oligoclonal bands & CSF protein electrophoresis abnr may (+)
• Etiologic dx made by virus isolation, PCR or acute & convalescent phase CSF Ab
titers
• Blood counts (N), leukopenia or mild leukocytosis
• Atypical lymphocytes in blood smeares & (+) heterophil (monospot) test = infx
mononucleosis
• Serum amylase elevated in mumps
Lange. Clinical neurology 7 edition
th
Treatment
• Except for herpes simplex encephalitis, no specific therapy
for viral meningitis and encephalitis is available.
• Headache and fever can be treated with acetaminophen, but
aspirin should be avoided, especially in children and young
adults (association with Reye syndrome)
• Seizures usually respond to phenytoin or phenobarbital.
• Supportive measures in comatose patients = mechanical
ventilation and IV or NGT feeding.

Reye Syndrome
• Reye syndrome is a rare disorder characterized by
encephalopathy or coma with laboratory evidence of hepatic
dysfunction.
• It usually occurs in children several days after a viral illness,
especially varicella or influenza B.
• Administration of salicylates appears to be an additional risk
factor.
• The incidence of Reye syndrome has declined dramatically in
recent years, at least partly as a result of vaccination for
varicella and the avoidance of aspirin in treating children
with febrile illnesses

HSV Encephalitis
• ~2/3 involve pts >40 yo
• Primary HSV infx  migrates along nerve axons  sensory
ganglia  persist in latent form  reactivated
• Neonatal HSV encephalitis usually results from acquisition of
type 2 during passage through birth canal w/ Mom (+) genital
lesion
• CNS involvement of HSV 2 in adults = meningitis >>>
encephalitis
Pathology
• HSV 1 = acute, necrotizing, assymetric hemorrhagic process +
lymphocytic & plasma cell rxn;
– usually involves medial temporal & inferior frontal lobes
• Intranuclear inclusion seen in neurons & glia
• Recover = cystic necrosis of involved regions
S&S Lab
• Headache, stiff neck, • Increased pressure
vomiting, behavioral • Pleocytosis (50-100 WBC/mL)
disorders, memory loss, • Mild prot elevation
anosmia, aphasia, • Normal glucose
hemiparesis, focal or • RBC, xanthochromia (yellowish
generalized seizure CSF; usually appear sev hrs after
• HSV encephalitis usually bleeding into subarachnoid space),
rapidly progressive over decreased glucose in some
several days  coma or cases
death • Cannot be isolated from CSF
• Most common sequelae in but DNA detected by PCR
pts survive = memory & • EEG: slow wave complexes arise
behavior disturbances from 1 or both temporal lobes
(predilection of HSV for
limbic structure)
• Th/ • Prognosis
– Most effective = – Pts <30 yo & lethargic
acyclovir 10-15 mg/kg IV only at onset of th/ =
every 8 hrs 14-21 days survive >> older
– Complication: erythema comatose pts
at infusion site, GI – Mortality rate ~25% at
disturbances, headache, 18 mo in pts + acyclovir
skin rash, tremor,
seizures,
encephalopathy or coma
– Th/ ASAP

Fungal Meningitis
• Fungi invade CNS  meningitis or focal PATHOGENESIS

intraparenchymal lesions
• Sev fungi = opportunistic organisms  infx
Fungi
in pts w/ Ca, corticosteroids,
immunosupressive drugs, debilitated hosts
• IV drug abuse = potential route for infx w/
hematogenous spread from
Candida & Aspergillus lungs, heart, GI, genitourinary
• Diabetic acidosis = strongly correlated w/ tract, skin
rhinocerebral mucormycosis
• Meningeal infx w/ Coccidioides,
Blastomyces, Actinomyces usually (+) in parameningeal sites (orbits,
paranasal sinuses)
healthy individuals
• Cryptococcus & Histoplasma infx can
occur in healthy or immunosuppressed
invade meninges (commonly
• Cryptococcal meningitis = most common mucormycosis, aspergillosis &
fungal infx in pts w/ HIV infx actinomycosis)

Clinical findings • S&S
– Headache & lethargy or confusion
• Subacute illness resembles TB – Nausea & vomiting, visual loss, seizure,
meningitis focal weakness
• Hx of predisposing condition: – Fever may be absent
– Ca – Diabetic pts + acidosis = facial or eye pain,
– Hemato malignancy nasal discharge, proptosis, visual loss 
– HIV infx urgent of Mucor infx
– Examine skin, orbit, sinuses, chest =
– Diabetes
evidence of systemic fungal infx
– Organ transplant – Neuro exam = meningeal irritation,
– Prolonged AB th confusional state, papilledema, visual loss,
– Corticosteroids or cytotoxic ptosis, exophthalmos, ocular or other CN
agents palsies, focal neuro abnr: hemiparesis
– Cryptococcus can cause sinal cord
– IV drug use
compression  evidence of spine
– Recent travel fungi endemic tenderness, paraparesis, pyramidal signs
in legs, loss of sensation over legs & trunk

• Lab findings
– Blood culture should be obtained • Treatment & prognosis
– Serum glucose & ABG lvl should be – Amphotericin B most common
determined in diabetic pts – Nephrotoxicity is common (force
– Urine should be examined for interruption of th/ for 2-5 days)
Candida – Newer lipid based formulations:
– CXR = hilar lymphadenopathy, Ampo B lipid
patchy or miliary infiltrates, complex/cholesteryl sulfate,
cavitation or pleural effusion liposomal ampho B = less
– CT or MRI = intracerebral mass nephrotoxic
lession assc w/ cryptococcus or – Coccidioides meningitis or not
others; a contiguous infx source in respond to IV th/ = intrathecal
orbit or paranasal sinuses or ampho B often added
hydrocephalus – 0,1 mg test dose diluted in 10 ml
– CSF pressure (N) or elevated CSF (+/- corticosteroids) 
– Fluid clear but viscous (cryptococci) increased to 0,25 – 0,5 mg every
– Aspergillus = PMN pleocytosis other day
– Micros w/ india ink = infecting – Mortality rates remain high in
organism fungal menignitis
– Mucormycosis = nasal mucosa
biopsy essential
Parasitic infx
Primary amebic Granulomatous amebic
meningoencephalitis encephalitis
• Free living amoeba Naegleria fowleri • Acanthamoeba/Hartmannella sp
• In prev healthy young pts exposed to • Occur w/ chronic illness or
polluted water immunosuppression
• Entry to CNS through cribriform plate  • Typically lasts for from 1 wk – 3 mo
diffuse meningoencephalitis affects • Char: subacute or chronic meningitis
base of frontal lobes & post.fossa & granulomatous encephalitis
• Char by: • Cerebellum, brain stem, basal
– Headache, fever, nausea, vomiting, signs ganglia, cerebral hemispheres
of meningeal irritation, disordered affected
mental status
• Acute confusional state = most
– CSF + PMN pleocytosis; elevated prot
common clinical finding
low glucose; high motile refractile
trophozoites on wet mount of • Sluggish motile trophozoites seen
centrifuged CSF on wet mount
– Fatal w/in 1 wk although th/ w/ • Successful th/: pentamidine,
amphotericin B 1 mg/kg/d IV effective sulfadiazone, flucytosine,
(may + azithromycin or clarithromycin) fluconazole, itranidazole
Lab & imaging
Cysticercosis • Peripheral blood eosinophilia, soft tissue
• Ingestion of larvae of pork calcification ,parasites in stool = dx
tapeworm (Taenia solium)  • CSF = lymphocytic pleocytosis (<100
affects brain 60-90% cases cells/mL) + eosinophils
• Larva  hematogen • Complement fixation & hemagglutination
dissemination  forms cyst in studies = assist dx
brain, ventricles & subarachnoid • CT or MRI = contrast enhaced mass lession
space + surrounding edema, intracerebral
• Neuro manif due to mass effect calcification or ventricular enlargement
of intraparenchymal cyst, TREATMENT
obstruction of CSF flow in • Abendazole 15 mg/kg/d 3 doses w/ meals
intraventricular cyst, 8 days _ anticonvulsants
inflammation causes basilar • Corticosteroid for increased ICP or lesion
meningitis near cerebral aqueduct or intraventricular
– Seizures, headache, focal foramina  hydrocephalus
neurologic signs, hydrocephalus,
• Single accessible lesion removed surgically
myelopathy, subacute meningitis
• Shunting for intraventricular lesion causing
hydrocephalus
Coma
• Pts incapable of being aroused • Sleeping & Coma
by external stimuli or inner – Sleeping persons may still
need respond to stimuli & capale of
• Deepest stage mental activity = dreams
(leaves traces of memory)
– No meaningful or purposeful
• Thus differing from stupor or
reaction of any kind coma
– Corneal, pupillary, pharyngeal
– Most important difference:
responses diminished
• Person sleep  stimulated  can
• Lighter stage be roused to normal & persistent
(semicoma/obtundation) consciousness
– Reflexes can be elicited – Physiologic differences:
• Cerebral O2 uptake doesn’t
– Plantar reflexes flexor/extensor
decrease during sleep (does in
(Babinski sign) coma)

Vegetative State
• Increase refinements in th/ of severe
systemic disease & cerebral injury  • Pts remains unresponsive, mostly
pts formerly would have died survived unconscious, don’t speak, no signs of
for indefinite period (w/out regaining awareness of environment or inner
any meaningful mental fx) need
• 1st – 2nd wk after cerebral injury = pts in • Motor activity limited to primitive
deep coma  Begin to open their eyes postural & reflex movements of
(1st response to painful stimuli)  limbs
spontaneously & for prolonged periods • Loss of sphincter control
• Pts may blink in response to threat or • May be arousal or wakefulness in
light & intermittently eyes move from alternating cycles = partial eye
side – side (following objects or fixating opening but neither regains awarness
momentarily on physician or family nor purposeful behavior
member) • BRAINSTEM FX PRESERVED,
• Respi quicken in response to CORTICAL (frontal & parietal cortex)
stimulation, certain automatism & thalamic injuries present
(swallowing, bruxism, grimacing,
grunting, moaning) may be observed

1 sign of vegetative state: • Initial days & wks,
• lack of consistent visual syndrome of
following of objects; unconscious awakening
• brief observation of = vegetative state
ocular movements is • Lasting for 3 mo after
subject to nontraumatic or 12 mo
misinterpretation  after traumatic injury =
repeated exam required persistent vegetative
1 important feature: state (PVS)
• lack of or minimal
change in EEG activity
during & after
stimulating pts
Minimally conscious state
• Less severe vegetative state but still profound
dementia
• Pts capable of some rudimentary behavior
– E.g; follows simple command, gesturing, produce
single words or brief phrases, inconsistent from 1
examination to another
• Preservation of ability to carry out basic motor
behaviors
• Either transitional or permanent
Akinetic Mutism
Locked-in Syndrome
• Known as pseudocoma • Pts are silent & inert due to
• Little or no disturbances of bilateral lesions (usually anterior
consciouness but only inability to parts of frontal lobes) leaving
respond adequately intact motor & sensory pathways
• Known as deefferented state • Pts profoundly apatetic, lacking
• Most often due to lesion of ventral extreme degree psychic drive or
pons (basis pontis) due to occlusion impulse to action (abulia)
of basilar artery  quadriplegia &
damages lower CN  inable to show Catatonia
facial expression, move, speak except • Pts unresponsive, in a state of stupor,
coded eye movement light coma or akinetic mutism
• Infarct  spares somatosensory • No signs of structural brain disease (no
pathways, ascending neuron system pupil or reflex abnr)
for arousal & wakefulness, midbrain • There is usually resistance to eye
(allows eyelids to raised) opening, some display waxy flexibility
• Lesion interrupts corticobulbar & of passive limb movement (flexibilitas
corticospinal pathways  deprived cerea) – immobile posture
pts speech & capacity to respond • (+) long period seemingly uncomfortable
except vertical gaze & blinking limb postures – rigidity (catalepsy)
Brain Death
• Central consideration in dx of
• State of coma in which brain
brain death:
was irreversibly damaged & – Absence of all cerebral fx
had ceased to fx, but – Absence of all brainstem fx
pulmonary & cardiac fx still (include: respi)
be maintained by artificial – Irreversibility of the state
means (coma depasse/state • Necessary to demonstrate
beyond coma) irrefutable cause of underlying
catastrophic brain damage:
• State of complete
– Trauma, cardiac arrest,
irresponsiveness to all cerebral hemorrhage
modes of stimulation, arrest TO EXCLUDE REVERSIBLE
of respiration and absence CAUSES: drug overdose,
of all EEG activity for 24 hrs extreme hypothermia

• Absence of brainstem fx judged by:
– Loss of spontaneous eye movements
• Dx of brain death: – Midposition of eyes
– Absence of cerebral fx – Lack response to oculocephalic & caloric
demonstrated by deep (oculovestibular) testing
coma & total lack of – Presence of dilated or midposition fixed
spontaneous pupils (not <3 mm)
movement & motor – Paralysis of bulbar musculature (no facial
and vocal responses to movement or gag, cough, corneal, sucking
visual, auditory, reflex)
cutaneous stimulation – Absence of motor & autonomic responses
– Spinal reflex may to noxious stimuli
persist, toes often flex – Absence respi movements
slowly in response to • Clinical findings:
plantar stimulation – Complete absence of brain fx
• Small or poorly reactive pupils
• Slight eye deviation + oculovestibular
stimulation
• Posturing of limbs
Test for Oculocephalic Reflex
Response (Doll’s Eyes Phenomenon).
A, Normal response—eyes turn

together to side opposite from turn
of head.
B, Abnormal response—eyes do not

turn in conjugate manner.
C, Absent response—eyes do not

turn as head position changes.
(A and C from Rudy EB: Advanced

neurological and neurosurgical
nursing, St Louis, 1984, Mosby.)
https://basicmedicalkey.com/alterations-in-cognitive-
systems-cerebral-hemodynamics-and-motor-function/
Test for Oculovestibular Reflex (Caloric Ice-Water Test).
A, Normal response—conjugate eye movements.

B, Abnormal response—dysconjugate or asymmetric eye movements.
C, Absent response—no eye movements.
Apnea test
A patient is considered to meet
apnea test criteria for brain
death if:
• No spontaneous respiratory • Treshold of max stimulation of
respi center in medulla oblongata
efforts were witnessed during PaCO2 60 mmHg
the test (as evidenced by • Pts w/ baseline hypercarbia
physical attempts to inspire or (COPD for example) assume
documentation of end-tidal maximal stimulation at PaCO2 20
carbon dioxide by bedside mmHg above baseline  pts w/
waveform analysis) intact brainstem demonstrate
spontaneous respi
AND
• The patient's PaCO2 is in
excess of 60 mmHg (or at least
20 mmHg above baseline)
http://www.surgicalcriticalcare.net/Guidelines/brain_death_determination_2009.pdf
Confirmatory tests in brain death
• Cerebral • Electroencephalography
angiography – Isoelectric or flat EEG
– Contrast medium (high – Dx of brain death until several hrs passed
pressure) in both from initial observation!
anterior & posterior • Exam performed at least ~6 hrs after
circulation injections precipitating event = evidence of
overwhelming brain injury from trauma or
– No intracerebral filling massive cerebral hemorrhage = no need
at lvl of carotid or serial testing
vertebral artery entry to • Cardiac arrest was antecedent event or cause
skull is unclear or drug or alcohol intoxication 
– Patent external carotid suppression of brainstem reflexes  wait
circulation ~24 hrs before repeat testing & pronouncing
pts is dead
– Possible delayed filling
• Possibility of reversible brain dysfx from
of superior longitudinal
toxins, drugs, hypothermia, hypotension!
sinus
– In children: determination not be made
before 7th postnatal day, period of
observation should be extended to 48 hrs
FIGURE 17-2 Appearance of Pupils at Different Levels of Consciousness.
Cortical Areas of the Left (Dominant) Hemisphere. (From Patton KT, Thibodeau GA: Anatomy & physiology, ed 8, St Louis, 2013, Mosby.)

Pemicu 2 Saraf

Uploaded by

Copyright:

Available Formats

You might also like

Pemicu 2 Saraf

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Pemicu 2 Saraf

Uploaded by

Copyright:

Available Formats

Penurunan Kesadaran

drowsiness maybe accompanied by

• Fever, tachycardia, HTN, sweating, Autonomic Often present Absent

William Howlett. Neurology in Africa. Available from: http://www.uib.no/filearchive/chapter9_neurology.pdf

Flinders university Clinical Skill Information Sheet

Adams & Victors Principles of Neurology

• Most common cause: insulin Clinical findings

• Symptoms: • The myopathy spares bulbar muscles

Lange. Clinical neurology 7th edition

• Symptoms: • Carpopedal spasm may occur

the facial (VII) nerve • Treatment

Encephalopathy. American College of Physicians. https://www.mnhospitals.org/Portals/0/Documents/patientsafety/Delirium/ACP%20Encephalopathy

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

• Complication of chronic alcoholism • Clinical findings

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

Adams & Victors Principles of Neurology

Adams & Victors Principles of Neurology

• Sudden swirling motion of brain induced by

Adams & Victors Principles of Neurology

torn BV, vasomotor contusion from contact

Adams & Victors Principles of Neurology

Adams & Victors Principles of Neurology

Lange. Clinical neurology 7th edition

The global burden of cerebrovascular disease. Thomas Truelsen. WHO

The global burden of cerebrovascular disease. Thomas Truelsen. WHO

The global burden of cerebrovascular disease. Thomas Truelsen. WHO

The global burden of cerebrovascular disease. Thomas Truelsen. WHO

Management of Raised Intracranial Pressure. Indian J Pediatr (2010) 77:1409–1416. http://medind.nic.in/icb/t10/i12/icbt10i12p1409.pdf

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

Adams & Victors Principles of Neurology

Indirectly lateral & downward displacement

creasing of lateral edge of

weakness & Babinski sign ipsilateral

Adams & Victors Principles of Neurology

Adams & Victors Principles of Neurology

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

Opioid • Cardinal features of opioid overdose

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

Lange. Clinical neurology 7th edition

Clinical Neurology. Lange. 7th edition

Clinical Neurology. Lange. 7th edition

Clinical Neurology. Lange. 7th edition

Clinical Neurology. Lange. 7th edition

• Gram-stained smears of CSF identify the causative organism in

Clinical Neurology. Lange. 7th edition

Clinical Neurology. Lange. 7th edition

corticosteroid th/, HIV infx, metastatic dissemination of

areas (Asia, Africa) or

Lange. Clinical neurology 7th edition