KULIAH NEUROLOGI

S. Purwoko, dr, SpS.

 COMA
 Definition : UNARAUSABLE UNRESPONSIVENESS
 Etiology:
Circulation → Stroke/Shock
Encephalomeningitis
Metabolism → Hepatic/Uremic Encephalopathy
Electrolyte/Endocrine Disturbance → Hyponatremia
Neoplasm → Brain Tumors
Trauma Capitis → Epi/Sub-Dural Hemorrhage
Epilepsy → Status Epilepticus
Drug Intoxication → Sedative-Hypnotic/Opioids
 COMA
CLINICAL ASSESSMENT

 Structural Brain Lesion vs Diffuse Encephalopathy

 Structural lesion
→Supra vs Infra-Tentorial Lesion
→ Signs of Rostro-Caudal deterioration
 COMA
Supra-Tentorial Infra-Tentorial Diffuse
Encephalopathy
•Usually Normal size •Midbrain lesion : •Usually Normal size
(3-4 mm) & reactive Midsized (±5 mm) & reactive
Pupil Size & • Trans-tentorial & unreactive •Opiates : pinpoint &
Light reaction Herniation : •Pontine : sometimes unreactive
Large (>7 mm) Pinpoint (1-1.5 mm) •Anticholinergics :
& unreactive & unreactive large & unreactive

Reflex Eye •Midbrain : •Usually Normal

movements Normal Impaired adduction •Impaired : Sedative/
(Doll’s eye •Pontine : Wernicke’s Encephalopathy
maneuver ) Impaired ad+abduction

•Usually Asymmetric
Motor •Symmetric: •Asymmetric: unilateral •Usually Symmetric
responses Trans-tentorial •Symmetric: bilateral •Asymmetric:Hypo/
Herniation Hyperglycemia/Hepatic Coma

Hallmark of Metabolic Encephalopathy: pupil reactive in the presence of impaired brainstem function
 COMA
Doll’s eye
Ventilatory Pupil Pupillary maneuver/ Gag Response to
Pattern Size response Caloric reflex Painful
Testing stimuli
Hemispheres Cheyne-Stokes Small (+) (+) (+) Purposeful/
Localizing
Early Normal Small (+) (+) (+) Purposeful/
Diencephalic (±2 mm) Localizing
Late Normal Small (+) (+) (+) Decorticate
Diencephalic
Midbrain Neurogenic Midsize (-) Adduction (+) Decerebrate
hyperventilation (±5 mm) (-)
Neurogenic ±5 mm/ (-)/(+) with Decerebrate/
Pons hyperventilation/ pinpoint magnifying Totally (-) (+) Flaccid (-)
Apneustic glass
Medulla Ataxic ±5 mm (-) Totally (-) (-) Flaccid (-)
(Oblongata)
COMA

Modified from Eka Musridharta, ,Initial Management of Trauma, Bali 2009

COMA

Modified from Eka Musridharta, Initial Management of Trauma, Bali 2009

 COMA
1. General Management (Supportive Treatment) :
* B1 to B6 (Breath-Blood-Brain-Bladder-Bowel-Bone)
* B1 (Breath) & B2 (Blood) = ABC (Airway-Breathing-Circulation)
* Breath : establishment of a clear airway & delivery of oxygen,
eg: insert Mayo tube
* Blood : maintained of a good perfusion
* Brain : a. Stop Seizure
b. Reduced Intra Cranial Pressure
b.1. 30° head elevation
b.2. Give Furosemide/Steroid/Osmotherapy
* Bladder: avoided urinary retension & maintained fluid balancing
* Bowel : avoided obstipation & maitained good nutrition
* Bone : prevent pressure sore

2. Specific Therapy
 COMA
DIFFERENTIAL DIAGNOSIS
1. Locked-in State
* Infarction of the basis pontis
* Paralysis of lower cranial nerve and limb muscles
with preserved alertness and respiration
* Communication through blinking or eye movements
and yes-or-no questions

2. Vegetative State
* Preservation of vegetative functions (sleep-wake cycles,
autonomic control and respiratory function)
* No evidence of inner or outer awareness
* Persistent → ≥1 month
 COMA
3. Brain Death
* No function of Cerebrum or Brainstem
* Cardiovascular is the only spontaneous activity
* Standards for determination of BRAIN DEATH
(President’s Commision for the Study of Ethical Problems in
Medicine and Biomedical and Behavioral Research 1981)
1. Unresponsiveness
2. Absent Brain Stem Reflexes
2.1. Pupillary/Corneal/Oropharyngeal/Oculocephalic (Doll’s
eye maneuver)/Vestibulo-ocular (Caloric test) → (-)
2.2. Apnea test → O2 100% + pCO2 60 mmHg → no breath
3. Irreversibility of Brain Dysfunction → The cause must be known
No sedative drug intoxication, hypothermia, neuromuscular blockade, shock.
4. Persistence of Brain Dysfunction → 6 hours with confirmatory flat
EEG/12 hours without confirmatory flat EEG/24 hours for anoxic Brain injury
 COMA

References :
1. Adams RD, Victor M. Coma and Related Disorders of Consciousness. In:
Principles of Neurology, 5th ed. McGraw-Hill, 1993: 300 – 318.
2. Aminoff MJ, Greenberg DA, Simon RP. Coma. In: Clinical Neurology, 3 rd ed.
Appleton & Lange, 1996: 255 – 306.
3. Brust JCM. Coma. In: Brust JCM. Current Diagnosis & Treatment in
Neurology. Lange Med Books/McGraw-Hill, 2007: 29 – 34.
4. Chandra B. Pandangan Umum mengenai Koma. In: Harsono, ed. Kapita
Selekta Neurologi. Gajah Mada University Press, 1993: 1 – 24.
5. Gilroy J. Coma. In: Basic Neurology, 3rd ed. McGraw-Hill, 2000: 61 – 70.
 STROKE

DEFINITION (WHO) :

Rapidly developing clinical signs of focal

(at times global) disturbance of cerebral function,
lasting for more than 24 hours or leading to death,
with no apparent cause other than vascular origin
 STROKE
CLASSIFICATION

STROKE

ISCHEMIC HEMORRHAGE

THROMBOSIS EMBOLISM INTRACEREBRAL SUBARACHNOID

 STROKE
CLASSIFICATION

STROKE

Infark Emboli
Infark
Thrombotic
Intra-Cerebral
Hemorrhage
Sub-Arachnoid
Hemorrhage
 STROKE
ISCHEMIC
ISCHEMIC
STROKE

REVERSIBLE
TRANSIENT ISCHEMIC
PROGRSSIVE STROKE COMPLETED STROKE
ISCHEMIC ATTACK NEUROLOGICAL
DEFICIT

RESOLVE
RESOLVE
COMPLETELY BECOME WORSE AND CLINICALLY
COMPLETELY
> 24 Hours – FEW WORSE STABLE
≤ 24 Hours
DAYS/WEEKS
 STROKE
ISCHEMIC
Pathophysiology
The rule of Hagen-Pouisseuille
Q : Cerebral Blood Flow
P : Perfussion pressure
Pxr⁴  r⁴ : diameter of the vessels
L : the length of the vessels
Q = ----------- X ------
n : Blood viscosity
Lxn 8  : Constanta
8
CBF : 50 – 60 ml/100 gr/mnt
 STROKE
ISCHEMIC
Atherosclerosis Timeline
Complicated
Foam Fatty Intermediate Fibrous Lesion/
Cells Streak Lesion Atheroma Plaque Rupture

Endothelial Dysfunction
From First From Third From Fourth
Decade
Adapted from Pepine CJ. Am J Cardiol. Decade
1998;82(suppl 10A):23S-27S. Decade
 STROKE
ISCHEMIC
Pathophysiology
50-55 mL/100 g/minute NORMAL

20 mL/100 g/minute EEG flat

Ischemic
15 mL/100 g/minute loss of SSER Penumbra

10 mL/100 g/minute Membrane Damage

(K⁺ Efflux & Na⁺/Ca⁺⁺ Influx)
5 mL/100 g/minute Neuronal Death
STROKE
ISCHEMIC
 STROKE
ISCHEMIC
Patophysiology
AEROBIC METABOLISM
Glucose + O₂ → H₂O + CO₂ + 38 ATP

ANAEROBIC METABOLISM
Glucose → 2 ATP + Lactic Acid
(Neurotoxic)
Sodium Pump Failure

Influx of Sodium Cell Edema

Efflux of Potassium
 STROKE
ISCHEMIC

CLINICAL FINDINGS

 Cardinal :

* HEMI-PARETIC/PLEGIC (Motor System)

* HEMI-AN/HYP/HYPER/PAR-ESTHESI (Sensory System)
* ALTERNANS HEMI-PARESIS
(Contra-lateral Hemiparesis with Ipsi-lateral Cranial nerve
palsy at the level of lesion → Brainstem Stroke)
 STROKE
ISCHEMIC

CLINICAL FINDINGS

 Specific :
1. Anterior Cerebral Artery
* Contra-lateral Hemiparesis with the Leg more affected
than the arm
* Urinary incontinence
* Lack of motivation, or agitation
 STROKE
ISCHEMIC
CLINICAL FINDINGS

 Specific :
2. Middle Cerebral Artery
* The Motor & Sensory deficits are greater in the Face &
Arm than in the leg
* Contra-lateral Hemiparesis with similarly affected in the
arm and leg (deep perforating artery = Lenticulostriate
artery)
* Aphasia (Dominant Hemisphere), or Hemineglect &
spatial disorders (Nondominant Hemisphere)
 STROKE
ISCHEMIC
CLINICAL FINDINGS
 Specific :

3. POSTERIOR CEREBRAL ARTERY

* Contra-lateral Homonymous Hemianopia with macular
sparring → Bilateral Infarction → True Tunnel Vision
* Alexia without Agraphia (dominant hemisphere)

4. VERTEBRO-BASILAR ARTERY
* Alternans Hemiparesis
* Ataxia/Vertigo/Dysphagia
* Decreased of Consciousness
 STROKE
ISCHEMIC
RISK FACTORS
MODIFIABLE ISCHEMIC BLEEDING
Arterial Hypertension (+) (+)
Diabetes Mellitus (+) (-)
Cardiac Disease (esp Atrial Fibrilation) (+) (-)
Hypercholesterolemia (+) (-)
Cigarette Smoking/Tobacco Use (+) (±)
Obesity (+) (-)
Alcohol Abuse (+) (±)
Drug Abuse (±) (+)
Oral Contraseptive Use (Estrogen) (+) (±)
Hyperhomocysteinemia (+) (-)
 STROKE
ISCHEMIC

OTHER MODIFIABLE RISK FACTORS:

 Infection & Inflammation

 Hematologic Disorders
 Malignancy (Leukemia)
 Migraine
 Sleep apnea & snoring.
 STROKE
ISCHEMIC

NON MODIFIABLE RISK FACTORS

 Age
 Gender/Sex → Men > Women
 Race → Blacks > Asians & Hispanics > Whites
 Family History/Genetic
 STROKE
ISCHEMIC

DIAGNOSIS
 HEAD CT-SCAN :
* the quickest & easiest initial examination that can be
differentiated between Ischemic and hemorrhage
* negative hyper-dense spot rules out ICH

 HEAD MRI/MRA
* The best for Ischemic Stroke, esp to look for
Brainstem Stroke
* Better than Head CT-Scan to ruled out Brain Tumor
 STROKE
ISCHEMIC

INFARCT THROMBOTIC INFARCT EMBOLI

 STROKE
ISCHEMIC
TREATMENT
 General:
* Supportive Treatment (B1–B6) + 5-No
* Brain:
a. Stop Seizure → Give Diazepam & Phenytoin iv
b. ↓ Intra Cranial Pressure
→ 30° head elevation
→ Osmotherapy (Manitol 0.5 – 1 g/kg every 4 – 6 hours)
* No Steroid, No Diuretic, No Anti-Hypertensive,
No Anti-Coagulant, No Glucose (maintained <200)
 STROKE
ISCHEMIC

TREATMENT

 Thrombolytic Therapy :
* Use recombinant tissue Plasminogen Activator (rt-PA)
* Indicated for patient with clearly defined time of onset
within 3 hours of start treatment
* Only for patient who meet the inclusion & exclusion
criteria used in the NINDS trial.
* The risk is bleeding trasformation
 STROKE
ISCHEMIC

TREATMENT

 Anti Platelets Aggregation :

* Aspirin/Clopidogrel/Ticlopidine/Dipyridamole/
Triflusal/Pentoxifylline
* Aspirin is the most widely used
* The most common side effects of Aspirin are
Gastritis, Peptic Ulcer & GI bleeding
* Elective operation: Stop the Drugs 3-7 days before
 STROKE
ISCHEMIC
TREATMENT
 Neuroprotective Agent :
* Calcium Antagonists: Nimodipine/Nicardipine
* Now is Not Recommended

 Anti-Hypertensive :
* Acute phase:
Avoiding antihypertensive Tx for the 1st 72 hours
→ BP usually ↓ without Tx over the 1st several hours or days
* Chronic phase:
↓ BP < 140/90 or How Low Can You Go with
Start Low Go Slow
 STROKE
ISCHEMIC
PREVENTION
 Controlled HYPERTENSION
* Hypertension is the most common & powerful factor
for Stroke
* Every 10-mm Hg increase in Systolic BP
→ the relative risk of Stroke ↑ 1.7 – 1.9
* ↓ Systolic BP to < 140 mm Hg
→ ↓ the risk of 1st Stroke by 40%
→ keep the BP < 140/90 (or < 130/80, if Diabetic)
 STROKE
ISCHEMIC

PREVENTION
 Controlled CARDIAC DISEASE
* Stroke risk is 2 X for pts with Coronary Artery Disease
* Stroke risk is 4 X for pts with Congestive Heart Failure
* Atrial Fibrillation is responsible for 50% of Embolic
Strokes

 Controlled DIABETES
* increased relative risk of Stroke between 1.6 – 6.0
 STROKE
ISCHEMIC
PREVENTION
 Controlled HYPERLIPIDEMIA
* Strongly associated with ↑ risk of CAD, but less so
with an ↑ risk of Stroke
* Subsequent studies found a > consistent association
between lipid abnormalities & Ischemic Stroke
* Use Statins → beyond lipid reducing effects
= stabilize atherosclerotic plaques
= enhance endothelial function & microvascular
blood flow, & neuroprotective agents
= anti-inflammatory, antithrombotic
 STROKE
ISCHEMIC
PREVENTION
 Cessation of SMOKING
* the biological effects of smoking:
= ↑ platelet aggregation
= ↓ vascular distensibility & compliance
= ↓ HDL levels
* the proportion of Strokes attributable to tobacco use
(current, previous, & 2nd hand) is nearly one third

 Treat the ALL OTHERS RISK FACTOR

 STROKE
ISCHEMIC
PROGNOSIS
 30 days mortality is ± 20%
 Annual mortality rates raging from 5 – 8%
 Recurrent risk in the 1st 30 days is 3 –10%
 Long term recurrent rates are 2 – 20% per year
 The majority of neurologic recovery occurs within
the 1st 3 – 6 months following Stroke
 Cognitive & Language deficits may continue to
improve dramatically for up to 2 years
 STROKE
ISCHEMIC
References :
1. Adams HP. Principles of Cerebrovascular Disease. McGraw-Hill,
2007.
2. Aminoff MJ, Greenberg DA, Simon RP. Stroke. In: Clinical Neurology,
3rd ed. Appleton & Lange, 1996: 255 – 287.
3. Caplan LR. Stroke: A Clinical Approach, 2nd ed. Butterworth-
Heinemann, 1993.
4. Fitzsimmons B-FM. Cerebrovascular Disease: Ischemic Stroke. In:
Brust JCM. Current Diagnosis & Treatment in Neurology. Lange Med
Books/McGraw-Hill, 2007: 100 – 125.
5. Hachinski V. Clinical Physiology of the Cerebral Circulation. In: Toole
JF. Cerebrovascular Disorders, 3rd ed. Raven Press, 1984: 19 – 36.
6. Henry GL,Little N, Jagoda A, Pellegrino TR, Quint DJ. Acute Focal
Neurologic Deficits. In: Neurologic Emergencies, 3rd ed. McGraw-Hill,
2010: 121 – 143.
 STROKE
INTRACEREBRAL HEMORRHAGE

ETIOLOGY/PATHOFISIOLOGY/PATHOGENESIS
 The most common underlying cause is HYPERTENSION
 Chronic Hypertension → structural changes in the wall of
penetrating arteries → micro-aneurysm of Charcot-Bouchard
→ rupture → bleeding intraparenchymal
 Acute Hypertension → sudden increase in BP → ICH in
normotensive or chronically hypertensive patients
 Normotensive & elderly → Cerebral Amyloid Angiopathy →
accumulation of amyloid β-protein within the walls of
small/medium-sized leptomeningeal & cortical arteries →
displace collagen & contractile elements → brittle & weakened
artery → spontaneous bleeding

Others: AVM, Congenital/Saccular Aneurysm, Anticoagulant Tx, ITP, DIC, etc.
 STROKE
INTRACEREBRAL HEMORRHAGE

CLINICAL FINDINGS

Location Coma Pupils Eye movements Sensorimotor Seizures

Disturbance
Putamen (+) Normal Ipsilateral Hemiparesis (-)
Deviation
Thalamus (+) Small + Downward + Hemisensory (-)
Sluggish Inward
Lobar (-) Normal Normal/ Hemiparesis/ (+)
Ipsilateral Hemisensory
Deviation
Cerebellum Delayed Small + Impaired late Gait Ataxia (-)
Reactive
Pons Early Pinpoint Absent Horizontal Quadriparesis (-)
 STROKE
INTRACEREBRAL HEMORRHAGE
CLINICAL FINDINGS

ICH SAH Ischemic

TIA (-) (-) (+)
Onset Activity Activity Rest
Duration Minute/hour Minute Hours
Headache (+) (++) (-)
Vomiting (+) (+) (-)
Decreased of Consciousness (+) (+) (-)
Neck Stiffness (-) (+) (-)
Hemiparesis severe (-)/mild Mild/moderate
Subhyaloid bleeding (-) (+) (-)
 STROKE
INTRACEREBRAL HEMORRHAGE
Diagnostic of Choice :
1. Head CT-Scan, because it is:
→ the quickest (takes about 1 minute)
→ the easiest (available for 24 hours)
→ the most accurate (negative result rules out ICH)
→ less expensive than Head MRI/MRA
2. Siriraj Stroke score → 90% predictive accuracy
* (2.5 X consciousness level) + (2 X headache) + (2 X vomiting) +
(0.1 X Diastolic pressure) – (3 X atheroma markers) – 12 = …
* > 1 = supra tentorial hemorrhage; < 1 = infarction
* consciousness level 0 = alert; 1= drowsy/stupor; 2 = coma
* headache/vomiting/atheroma markers (+) = 1; (-) = 0
* atheroma markers : DM, angina, or peripheral vascular disease
(+) =1; (-) = 0
 STROKE
INTRACEREBRAL HEMORRHAGE
Diagnostic of Choice :

INTRACEREBRAL HEMORRHAGE SUBARACHNOID HEMORRHAGE

 STROKE
INTRACEREBRAL HEMORRHAGE
Differential Diagnosis :
1. Ischemic Stroke
2. Traumatic Intracranial Hemorrhage
2.1. Epidural Hematoma
* Classic: Lucid interval (+)
* Young adults → dura becomes ↑ adherent to the skull
with advanced age → rarely in the elderly
2.2. (Chronic) Subdural Hematoma
* Classic: conscious but confused with waxing & waning of
symptoms
* History of trauma could negative, or trivial
3. Subarachnoid Hemorrhage
4. Hypertensive Encephalopathy
 STROKE
INTRACEREBRAL HEMORRHAGE
Treatment :
1. General Supportif Treatment (B1 to B6)
Decreased Systolic BP 20% within or ≤ 160 mmHg is wise
(no evidence that modest lowering BP has deleterious effect)
Note : sublingual nifedipine contraindicated in all Stroke syndromes

2. Surgical Treatment
2.1. Indicated (Yatsu, 1995) :
2.1.1. Hematoma volume between 30 and 80 cc.
2.1.2. GCS between 7 and 10.
2.1.3. Lobar Hemorrhage
2.1.4. Cerebellar hemorrhage > 1.5 cm with 4th ventricular
distortion and/or ventricular enlargement
2.1.5. Cerebellar hemorrhage > 1.5 cm with reduction in
sensorium and/or gaze palsy
 STROKE
INTRACEREBRAL HEMORRHAGE
Treatment :
2. Surgical Treatment
2.2. AHA Guidelines 1999

Therapeutic CRITERIA
Approach
1. Pts with cerebellar hemorrhage > 3 cm who are neurologically deteriorating
or who have clinical or radiographic evidence of symptomatic brainstem
compression or hydrocephalus from ventricular obstruction
Surgical Candidates 2. ICH associated with aneurysm, AVM, or cavernous malformation, if pts have
a chance for good outcome and lesion is surgically accessible
3. Young pts with moderate or large lobar hemorrhage who are clinically
deteriorating
Non-Surgical 1. Pts with small hemorrhages or minimal neurologic deficits
Candidates 2. Pts with a GCS < 5, except for cerebellar hemorrhages with brainstem
compression
Best Therapy Unclear All other patients
 STROKE
INTRACEREBRAL HEMORRHAGE

Complications :
1. Gastrointestinal hemorrhage → within the 1st week
2. SIADH (Syndrome of Inappropriate secretion of AntiDiuretic
Hormone) → Hyponatremia
3. Brain herniation

Prognosis :
 30 – 70% die in 1 to 30 days
 Survivors sometimes achieve a surprisingly good recovery,
since the hemorrhage has to some extent pushed brain
tissue aside rather than destroying it.
 STROKE
INTRACEREBRAL HEMORRHAGE

References :
1. Adams RD, Victor M. Cerebrovascular Diseases. In: Principles of Neurology,
5th ed. McGraw-Hill, 1993: 669 – 748.
2. Allah A, Kuswara FF, Limoa A, Wuysang G. Gangguan Peredaran darah Otak
(Stroke). In: Harsono. Kapita Selekta Neurologi. Gajah Mada University
Press, 1993: 25 – 47.
3. Aminoff MJ, Greenberg DA, Simon RP. Stroke. In: Clinical Neurology, 3 rd ed.
Appleton & Lange, 1996: 255 – 287.
4. Bernstein RA. Cerebrovascular Disease: Hemorrhagic Stroke. In: Brust JCM.
Current Diagnosis & Treatment in Neurology. Lange Med Books/McGraw-
Hill, 2007: 126 – 147.
5. Gilroy J. Intracerebral, Pontine, and Intracerebellar Hemorrhage. In: Basic
Neurology, 3rd ed. McGraw-Hill, 2000: 297 – 306.
6. Yatsu FM, Grotta JC, Pettigrew LC. Stroke: 100 Maxims. Edward Arnold,
1995.
 STROKE
SUBARACHNOID HEMORRHAGE
PATHOLOGY/PATHOGENESIS/PATHOPHYSIOLOGY
 80% is caused by rupture of Saccular aneurysm =
(Congenital) berry aneurysm (inherited weakness of the vessel
wall, especially at sites of branching)
 85 - 95% of berry aneurysm occur in the anterior
portion of the circle of Wilis
 5 - 10% is caused by rupture of AVM
 Rupture → acute elevation of blood pressure
→ ↑ ICP → distorts pain sensitive structure
→ headache
→ ↓ CBF → ↓ consciousness
→ subhyaloid retinal hemorrhage
 STROKE
SUBARACHNOID HEMORRHAGE
EPIDEMIOLOGY :
 5 – 10% of all Strokes
 Occurs between ages 40 – 60, with peak

between ages 55 – 65

Symptoms & Signs

 Classic : “The worst headache I ever had in my life”
 1/3 onset occurs during physical exertion
 2/3 onset occurs during sleep or ordinary daily
activities
 STROKE
SUBARACHNOID HEMORRHAGE
Symptoms & Signs
 Sentinel headache (sudden onset severe headache that reaches
max intensity in seconds, and last for a few hours to a week)
→ Days or weeks before
 Hunt and Hess Grading Scale

Grade Characteristic Genuine

1 Headache Asymptomatic or with slight headache and stiff neck

2 Meningeal signs, severe Moderate to severe headache and nuchal rigidity

but no focal or lateralizing neurologic signs
headache, cranial neuropathy
Lethargy; inattentiveness,
Drowsiness, confusion, and mild focal deficit
3 requiring repeated stimulation to
remain alert; hemiparesis
4 Stupor; brief arousal only to Persistent stupor or semicoma, early decerebrate
rigidity and vegetative disturbances
painful stimulus
5 Coma-no arousal to any stimulus Deep Coma and decerebrate rigidity
 STROKE
SUBARACHNOID HEMORRHAGE
Diagnostic Studies
 Head CT-Scan → sensitivity 95% within 1st 12 hours
 CT-Scan (-) → Lumbar Puncture
 Identifying the source of hemorrhage
* Catheter Angiography → 4 vessel cerebral
arteriography
* Computed Tomographic Angiography (CTA)
→ safety, rapidity, convenience & high sensitivity
* Magnetic Resonance Angiography (MRA)
→ not sufficiently sensitive to detect small
ruptured aneurysm
 STROKE
SUBARACHNOID HEMORRHAGE

Differential Diagnosis

1. Traumatic SAH → usually over the brain convexity

and not in the basal cisterns
2. Intracerebral Hemorrhage
3. Acute Meningitis
4. Hypertensive Encephalopathy → hypertensive
retinopathy + no nuchal rigidity
 STROKE
SUBARACHNOID HEMORRHAGE

TREATMENT :

1. Medical Management
* General supportive treatment
* Reduce BP to ± systolic 160 mmHg, but prevent from
hypotension
* Nimodipine 60 mg every 4 hours for 21 days
Carefull with hypotension (main adverse effect)
* Prophylactic anticonvulsant is a wise option
 STROKE
SUBARACHNOID HEMORRHAGE

TREATMENT :

2. Surgical Treatment
* Hunt & Hess grades 1-3
* Early intervention (within 2 days after the onset)
* For obliterate ruptured aneurysm & prevent
rebleeding
 STROKE
SUBARACHNOID HEMORRHAGE
COMPLICATIONS :
1. Rebleeding
* 4 – 10% in the 1st 24 – 48 hours after then onset with a
mortality rate of 70%
* The risk in the 1st month after rupture is ± 30%
2. Vasospasm
* The incidence is 30%
* Most common between days 4 – 14, with peaks by days
10 – 14, and spontaneously resolving after 21 days of
rupture aneurysm
* The mortality rate is 14 – 20%
 STROKE
SUBARACHNOID HEMORRHAGE

COMPLICATIONS :
3. Hydrocephalus
4. Seizures occur in 10 – 20% of cases

PROGNOSIS
 10 – 20 % die before reaching a hospital
 25 – 30% die within the 1st 24 hours, 25 – 50% die
within 30 days & another 25% die after 3 months
 The risk of rebleeding in survivors is ↓ after 6 mo
 STROKE
SUBARACHNOID HEMORRHAGE

References :
1. Adams RD, Victor M. Cerebrovascular Diseases. In: Principles of Neurology,
5th ed. McGraw-Hill, 1993: 669 – 748.
2. Allah A, Kuswara FF, Limoa A, Wuysang G. Gangguan Peredaran darah Otak
(Stroke). In: Harsono. Kapita Selekta Neurologi. Gajah mada University
Press, 1993: 25 – 47.
3. Aminoff MJ, Greenberg DA, Simon RP. Stroke. In: Clinical Neurology, 3 rd ed.
Appleton & Lange, 1996: 255 – 287.
4. Bernstein RA. Cerebrovascular Disease: Hemorrhagic Stroke. In: Brust JCM.
Current Diagnosis & Treatment in Neurology. Lange Med Books/McGraw-
Hill, 2007: 126 – 147.
5. Gilroy J. Subarachnoid Hemorrhage. In: Basic Neurology, 3 rd ed. McGraw-
Hill, 2000: 279 – 295.
HYPERTENSIVE ENCEPHALOPATHY
Definition :
A syndrome characterized by marked elevation of BP and
evidence of increased ICP

Etiology & Pathology

 Most pts have a history of essential Hypertension
 Secondary to another diseases : Renal disease,
Pheochromocytoma, or Toxemia Gravidarum
 Diffuse cerebral edema & cerebral vasospasm
→ impaired autoregulation of CBF → small infarcts
& petechial bleeding → mostly in the Brainstem
HYPERTENSIVE ENCEPHALOPATHY

Symptoms & Signs

 Severe Headache, nausea-vomiting, visual

disturbances, altered mental status (confusion-
stupor), focal neurologic deficits & seizures
 BP > 250/150 mmHg (in pts with chronic HT)
 Lower BP in normotensive pts
 Ophthalmoscopy : Hypertensive retinopathy Grd-4
HYPERTENSIVE ENCEPHALOPATHY
Laboratory Examination :
 Renal function test
 Head CT-Scan
 Lumbar puncture → Normal/↑ CSF pressure & protein

Differential Diagnosis :
 Diagnosis of exclusion
 Stroke (Ischemic & Hemorrhage)
HYPERTENSIVE ENCEPHALOPATHY
TREATMENT:
 Rapid resolution occurs when the BP is lowered
 In the 1st hour, diastolic BP should not ↓ < 100

PROGNOSIS :
 Untreated → Stroke, Coma, and Death
 Prompt treatment → full clinical recovery
HYPERTENSIVE ENCEPHALOPATHY

References :
1. Adams RD, Victor M. Cerebrovascular Diseases. In: Principles of
Neurology, 5th ed. McGraw-Hill, 1993: 734 - 735.
2. Aminoff MJ, Greenberg DA, Simon RP. Disorders of Cognitive Function:
Approach to Diagnosis & Acute Confusional States. In: Clinical
Neurology, 3rd ed. Appleton & Lange, 1996: 40 – 41.
3. Jay CA. Systemic & Metabolic Disorders. In: Brust JCM. Current
Diagnosis & Treatment in Neurology. Lange Med Books/McGraw-Hill,
2007: 497 – 498.
4. Gilroy J. Cerebrovascular Disease. In: Basic Neurology, 3rd ed. McGraw-
Hill, 2000: 262 – 263.
 APHASIA
 Loss/impairment of language function as a
result of Brain damage in language-dominant
hemisphere

 90% people are right handed

→ 95% process language in the left cerebral
hemisphere/dominance

 10% people with left handed

→ 60% have left cerebral dominance
 APHASIA

 Aphasias with impaired repetition

Type Naming Fluency Auditory Location of lesion
Comprehension

Broca’s (±) (-) (+) 44 & 45

Wernicke’s (-) (+) (-) 22
Global (-) (-) (-) Left Hemisphere
Conduction (±) (+) (+) Arcuate fasciculus
 APHASIA

 Aphasias with preserved repetition

Type Naming Fluency Auditory Location of lesion
Comprehension
Motor (-) (-) (+) Surrounding Broca’s
transcortical area
Sensory (-) (+) (-) Surrounding
transcortical Wernicke’ s area
Mixed (-) (-) (-) Surrounding Broca’s
transcortical and Wernicke’s
Anomic (-) (+) (+) Anywhere within left
(or right) hemisphere
 APHASIA

References :

1. Adams RD, Victor M. Affection of Speech and Language. In: Principles of

Neurology, 5th ed. McGraw-Hill, 1993: 411 – 430.
2. Brust JCM. Aphasia, Apraxia & Agnosia. In: Current Diagnosis & Treatment
in Neurology. Lange Med Books/McGraw-Hill, 2007: 35 – 36.
3. Waxman SG, deGroot J. Higher Cortical Function. In: Correlative
Neuroanatomy. Appleton & Lange, 1995: 267 – 269.
 DEMENTIA
DEFINITION
 A clinical syndrome composed of an acquired,
generalized of failing memory and impaired of
other intellectual functions (orientation, thinking,
comprehension, calculation, capacity for learning,
language, judgment, executive function &
visuospatial function) due to chronic progressive
degenerative disease of the brain

 Affect the content, but not the level of

consciousness
 DEMENTIA

DEMENTIA

CORTICAL SUBCORTICAL

FRONTO Progressive Normal

ALZHEIMER VASCULAR
TEMPORAL Supranuclear Pressure
DISEASE DEMENTIA
DEMENTIA Palsy Hydrocephalus
 DEMENTIA
Feature Cortical Dementia
Damage to cortical neurons,
Patophysiology usually degenerative
• Confusion & memory loss > • Confusion & memory loss <
Clinical • Apraxia & language
features difficulties are common
Important • Alzheimer’s disease
causes • Frontotemporal dementia
• Creutzfeldt-Jakob disease
Subcortical Dementia
• Damage to white matter &
subcortical gray matter
• Can be vascular,
inflammatory, or
degenerative
• Gait & coordination deficits
are common
• Vascular dementia
• Multiple sclerosis
• Progressive Supranuclear
Palsy
 DEMENTIA

Cognitive Function Cortical Dementia Subcortical Dementia

Attention & Concentration Intact Impaired

Speed of Mental Processing Normal Slow

Language Skills Impaired Relative Intact, incld naming

Orientation to Time & Place Impaired Often Preserved

Memory (Short-term Recall) Impaired Storage Impaired Retrieval

 DEMENTIA

Movement Cortical Dementia Subcortical Dementia

Speed of Movement Normal Slow

Gait Normal Slow

Sense of Equilibrium Normal Imbalanced

Posture Normal Stooped

 DEMENTIA

Diagnostic Tests
 Laboratory Examination
CBC, glucose, LFT, RFT, serum electrolytes, Thyroid
function, B12 & folate levels, & syphilis serology
 Neuroimaging
CT-Scan, MRI, PET-Scan & SPECT
 Neuropsychological testing
 DEMENTIA

Potentially Treatable Causes of Dementia

 Infections
→ HIV encephalitis; Neurosyphilis; Creutzfeldt-Jakop
disease
 Metabolic & Toxic
→ Hypothyroidism; Hepatic or Renal failure;
Psychoactive medications; B12 or folate deficiency;
Alcoholism
 Neoplastic → Brain tumors; Carcinomatosis
 Other → Normal Pressure Hydrocephalus
 DEMENTIA
ALZHEIMER DISEASE

Essential of Diagnosis
 Insidious onset and gradual progression of memory loss
 Short-term memory impairment and forgetfulness
 Impairment of one or more other cognitive domains,
including aphasia, apraxia, agnosia, or executive functioning

Dementia Evaluation
 Screening with Mini Mental State Examination (MMSE)
 Laboratory studies to look for treatable disorders
 Neuroimaging studies with Head CT-Scan or MRI
PET or SPECT not available in Indonesia
 DEMENTIA
ALZHEIMER DISEASE

Differential Diagnosis
1. Delirium → rapid deterioration + fluctuating of alertness
2. Other Dementias: VD/NPH, etc

TREATMENT
3. Cholinesterase inhibitors:
Donepezil/Rivastigmine/Galantamine
4. NMDA receptor antagonists: Memantine
 DEMENTIA
VASCULAR DEMENTIA

Essential of Diagnosis
 Cognitive change has a subcortical typology
 Decreased concentration, slowed thinking (bradyphrenia), and
deficits in executive function (initiate, plan and organize)
 Clinical Strokes with radiologic evidence of cerebral infarcts
 Multiple large-vessel infarcts (Multi-infarct Dementia) and
Small-vessel ischemic disease/Binswanger Disease (multiple
lacunes in the basal ganglia/subcortical/periventricular white
matter)
 Evidence of relationship between the Dementia & Stroke(s)
 Motor dysfunction, sometimes including gait disorder
 Urinary dyscontrol, typically incontinence or frequency
 DEMENTIA
VASCULAR DEMENTIA
Diagnostic Criteria
 No Radiologic or Laboratory findings confirm specifically
 Typically pts may have deficits in executive function including
decreased speed of processing and difficulty with initiation
 The absence of pathologic changes characteristic of AD or
another neurodegenerative condition on autopsy
 Hachinski scale is ≥ 7

Prevention & Treatment :

 Primary or secondary prevention of Stroke is the key
 Few studies have examined the efficacy of cholinesterase
inhibitors and Memantine
 DEMENTIA
VASCULAR DEMENTIA
HACHINSKI Scale
Abrupt onset of neurological symptoms 2 points

History of focal neurological symptoms 2 points

History of focal neurological signs 2 points

History of Stroke 2 points

Fluctuating course of symptoms 2 points

Stepwise neurological deterioration 1 point

Nocturnal confusion 1 point

Relative preservation of personality 1 point

Depression 1 point

Prominent somatic complaints 1 point

Pseudobulbar affect 1 point

≥ 7 points suggests Vascular
History Dementia, & ≤ 4 points suggests Alzheimer’s
of hypertension Disease
1 point
 DEMENTIA
NORMAL PRESSURE HYDROCEPHALUS

Essential of Diagnosis
 Triad of symptoms: gait (ataxic), bladder function
(incontinent) & mentation (dementia)
 Gait disorder, typically wide-based “magnetic” gait, with short
stride → the most frequent symptom
 Urinary dyscontrol, typically incontinence or frequency and
urgency
 Cognitive change or Dementia, typically subcortical in nature
 Cognitive symptoms usually occur after the onset of gait and
urinary dysfunction
 Ventricular enlargement without commensurately enlarged
sulci
 DEMENTIA
NORMAL PRESSURE HYDROCEPHALUS
 DEMENTIA
NORMAL PRESSURE HYDROCEPHALUS
Diagnosis of Choice :
 Head CT-Scan, or preferably MRI
 Ventricular enlargement out of proportion to peripheral sulcal
enlargement

Special Test :
Determining the likelihood of responsiveness of the syndrome
to CSF shunting with large-volume (40 mL) Lumbar Puncture

TREATMENT :
VP (Ventriculo-Peritoneal) shunt
 DEMENTIA
MILD COGNITIVE IMPAIRMENT
Essential of Diagnosis
 Subjective memory complaints
 Objective evidence of memory impairment→ impaired delayed recall
performance or difficulty benefiting from semantic cues during learning or
recall
 Normal function in activities of daily living
 Preserved general cognitive function
 Not a disease but is considered to be transitional state between
normal cognitive function and AD

Special Test :
MMSE not useful → Formal Cognitive test

TREATMENT : no specific therapies

 DEMENTIA
References :
1. Adams RD, Victor M. Dementia & the Amnesic (Korsakoff) Syndrome. In:
Principles of Neurology, 5th ed. McGraw-Hill, 1993: 364 – 377.
2. Aminoff MJ, Greenberg DA, Simon RP. Disorders of Cognitive Function:
Dementia & Amnestic Syndromes. In: Clinical Neurology, 3 rd ed. Appleton &
Lange, 1996: 48 – 70.
3. Gilroy J. Degenerative Diseases. In: Basic Neurology, 3 rd ed. McGraw-Hill,
2000: 343 - 392.
4. Marder K. Dementia & Memory Loss. In: Brust JCM. Current Diagnosis &
Treatment in Neurology. Lange Med Books/McGraw-Hill, 2007: 78 – 99.
5. Misulis KE, Head TC. Disorders-Mental Status. In: Netter’s Concise
Neurology. Elsevier Saunders, 2007: 116 – 142.
6. Alzheimer’s disease & Dementia. In: MIMS Neurology & Psychiatry
Indonesia 2nd ed, 2010/2011: 1 – 11.