S. Purwoko, dr, SpS.

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
CLINICAL ASSESSMENT

Structural Brain Lesion vs Diffuse Encephalopathy

Structural lesion
Supra vs Infra-Tentorial Lesion
Signs of Rostro-Caudal deterioration
 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/
(Dolls eye Pontine : Wernickes 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
 Dolls 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)
Modified from Eka Musridharta, ,Initial Management of Trauma, Bali 2009
Modified from Eka Musridharta, Initial Management of Trauma, Bali 2009
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
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
3. Brain Death
* No function of Cerebrum or Brainstem
* Cardiovascular is the only spontaneous activity
* Standards for determination of BRAIN DEATH
(Presidents 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 (Dolls
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
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, 3rd 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.
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
CLASSIFICATION

STROKE

ISCHEMIC HEMORRHAGE

THROMBOSIS EMBOLISM INTRACEREBRAL SUBARACHNOID

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
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 -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.
CLINICAL FINDINGS

Location Coma Pupils Eye movements Sensorimotor Seizures

Disturbance

Putamen (+) Normal Ipsilateral Deviation Hemiparesis (-)

Thalamus (+) Small + Downward + Hemisensory (-)

Sluggish Inward
Lobar (-) Normal Normal/ Hemiparesis/ (+)
Ipsilateral Deviation Hemisensory
Cerebellum Delayed Small + Impaired late Gait Ataxia (-)
Reactive
Pons Early Pinpoint Absent Horizontal Quadriparesis (-)
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 (-) (+) (-)
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
Diagnostic of Choice :

INTRACEREBRAL HEMORRHAGE SUBARACHNOID 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
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
 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
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.
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, 3rd
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.
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
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
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

headache, cranial neuropathy but no focal or lateralizing neurologic signs

Lethargy; inattentiveness,
3 requiring repeated stimulation to
remain alert; hemiparesis
4 Stupor; brief arousal only to
painful stimulus
Drowsiness, confusion, and mild focal deficit
Persistent stupor or semicoma, early decerebrate
rigidity and vegetative disturbances

5 Coma-no arousal to any stimulus Deep Coma and decerebrate rigidity

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
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
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
TREATMENT :

2. Surgical Treatment
* Hunt & Hess grades 1-3
* Early intervention (within 2 days after the onset)
* For obliterate ruptured aneurysm & prevent
rebleeding
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%
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
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, 3rd
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, 3rd ed. McGraw-
Hill, 2000: 279 295.
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
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
Laboratory Examination :
Renal function test
Head CT-Scan
Lumbar puncture Normal/ CSF pressure & protein

Differential Diagnosis :
Diagnosis of exclusion
Stroke (Ischemic & Hemorrhage)
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
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.
 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
The great majority of aphasic px of any type have
impaired writing, & over time, can improve
agraphia is the only residual abnormality
 Aphasias with impaired repetition
Type Naming Fluency Auditory Location of lesion
Comprehension

Brocas () (-) (+) 44 & 45

Wernickes (-) (+) (-) 22
Global (-) (-) (-) Left Hemisphere
Conduction () (+) (+) Arcuate fasciculus
 Aphasias with preserved repetition
Type Naming Fluency Auditory Location of lesion
Comprehension
Motor (-) (-) (+) Surrounding Brocas
transcortical area
Sensory (-) (+) (-) Surrounding
transcortical Wernicke s area
Mixed (-) (-) (-) Surrounding Brocas
transcortical and Wernickes
Anomic (-) (+) (+) Anywhere within left
(or right) hemisphere
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.
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

CORTICAL SUBCORTICAL

FRONTO Progressive Normal

ALZHEIMER VASCULAR
TEMPORAL Supranuclear Pressure
DISEASE DEMENTIA
DEMENTIA Palsy Hydrocephalus
 Feature Cortical Dementia Subcortical Dementia
Damage to cortical Damage to white matter
Patophysiology neurons, usually & subcortical gray matter
degenerative Can be vascular,
inflammatory, or
degenerative
Confusion & memory loss Confusion & memory loss
Clinical features Apraxia & language Gait & coordination
difficulties are common deficits are common
Vascular dementia
Important Alzheimers disease Multiple sclerosis
causes Frontotemporal dementia Progressive Supranuclear
Creutzfeldt-Jakob disease Palsy
Huntingtons disease
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
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
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
Differential Diagnosis
1. Delirium rapid deterioration + fluctuating of alertness
2. Other Dementias: VD/NPH, etc

TREATMENT
1. Cholinesterase inhibitors:
Donepezil/Rivastigmine/Galantamine
2. NMDA receptor antagonists: Memantine
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
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
 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
History of hypertension 1 point
Evidence of atherosclerosis 1 point

7 points suggests Vascular Dementia, & 4 points suggests Alzheimers Disease

Essential of Diagnosis
Triad of symptoms: gait, mentation & bladder function
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
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
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

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, 3rd ed. Appleton
& Lange, 1996: 48 70.
3. Gilroy J. Degenerative Diseases. In: Basic Neurology, 3rd 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: Netters Concise
Neurology. Elsevier Saunders, 2007: 116 142.
6. Alzheimers disease & Dementia. In: MIMS Neurology & Psychiatry
Indonesia 2nd ed, 2010/2011: 1 11.