Flexor spasms, clonus Present Absent

A stroke (cerebrovascular accident is a vague term which should be avoided) is defined as a

syndrome of rapid (abrupt) onset of a neurologic deficit that is attributable to a focal vascular cause

(Flowchart 6E.2). World Health Organization (WHO) definition: Stroke is a “rapidly developing clinical signs of focal (or

global) disturbance of cerebral function, with symptoms lasting for 24 hours or longer or leading to

death, with no apparent cause other than of vascular origin”.

Progressing stroke (or stroke in evolution): It is a stroke in which the focal neurological deficit

worsens after the patient first presents. It may be due to increasing volume of infarction, secondary

hemorrhage in the infarcted area, or increasing cerebral edema.

Complete stroke: Rapid onset with persistent focal neurological deficit which does not progress

beyond 96 hours.

Evolving stroke: Gradual stepwise development of neurological deficits. Focal cerebral deficits that

develop slowly (over weeks to months) are unlikely to be due to stroke and are more suggestive of

tumor or inflammatory or degenerative disease.

Terminologies

Several terms are used to classify strokes mainly based on the duration and evolution of symptoms.

Transient ischemic attack (TIA): Described later

Reversible ischemic neurological deficit (RIND): In some cases, deficits last for longer than 24

hours but resolve completely or almost completely within a few days.

Stuttering hemiplegia: Internal carotid lesions are characterized by repeated episodes of TIA

followed by fully evolved stroke.

Flowchart 6E.2: Types of stroke.

Table 6E.2: Risk factor for stroke.

Risk factors in patients of all age groups

High-risk

Hypertension (including

isolated systolic)

Smoking

Diabetes mellitus

Atrial fibrillation

Drugs: Cocaine,

amphetamine

Dilated cardiomyopathy

Endocarditis

High cholesterol

Obesity

Vasculitis: Systemic vasculities [e.g. polyarteritis nodosa—PAN), granulomatosis with

polyangiitis (Wegener’s) etc.], primary CNS vasculitis

Meningitis (syphilis, tuberculosis, fungal, bacterial, zoster)

Low-risk

Migraine Recent myocardial infarction

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

–

–

–

–

–

–

–

•

–

•

–

–

–

–

–

•

–

-

-

-

-

-

-

-

-

–

-

-

-

-

-

-

Oral contraceptives or alcohol

Patent foramen ovale

Prosthetic valve

Sleep apnea

Additional risk factors that are more common in young patients

Hypercoagulable disorders

Protein C and S deficiencies

Antithrombin III deficiency

Antiphospholipid antibody

syndrome

Factor V Leiden mutation

Prothrombin G20210A

heterozygous mutation

Sickle-cell anemia

Hyperhomocysteinemia

Thrombotic thrombocytopenic purpura

Arterial dissection

Infections (e.g. syphilis, HIV)

Systemic malignancy

(CNS: central nervous system; HIV: human immunodeficiency virus)

Table 6E.3: Causes for young stroke.

Cardiac

Congenital heart disease, patent foramen ovale

Atrial myxoma

Atrial fibrillation and other arrhythmia

Cardiomyopathy, myocarditis, myocardial

infarction

Cardiac surgery, cardiac catheterization

Endocarditis, rheumatic heart disease

Prosthetic valve

Hematologic

Sickle cell disease, iron deficiency anemias,

polycythemia vera

Hypercoagulable states

Inherited prothrombotic states, protein C and S

deficiency, antithrombin III deficiency, factor V

Leiden gene mutation, prothrombin gene mutation

Antiphospholipid antibody syndrome

Hyperhomocysteinemia

Myeloproliferative disorders (e.g. leukemia,

lymphoma)

Pregnancy exposure to hormonal treatments,

such as anabolic steroids and erythropoietin,

nephrotic syndrome

Vascular

Noninflammatory

Arterial dissection

Secondary to connective tissue disease (Ehlers-Danlos, Marfan)

Moyamoya disease

Hypertension

Radiation vasculopathy

Vasculitis and postinfectious vasculopathy

Migraine

Cerebral autosomal dominant arteriopathy with subcortical

infarcts and leukoencephalopathy (CADASIL) Fibromuscular

dysplasia, Susac’s syndrome, Sneddon’s syndrome, Fabry’s

disease

Inflammatory

Takayasu arteritis

Giant cell arteritis

Kawasaki disease

Polyarteritis nodosa

Human immunodeficiency virus (HIV)

Bacterial meningitis

Illicit drug use: Cocaine, amphetamine

Table 6E.4: Differences between hemorrhagic, thrombotic, and embolic strokes.

Feature Hemorrhagic stroke (Intracerebral

or subarachnoid hemorrhage)

Ischemic stroke

Thrombotic Embolic

Time of onset of stroke During activity Suddenly and often during sleep

or in the early morning (4 AM)

Any time (usually during

activity)

Rapidity of onset and

progression

Over minutes and hours On waking up or over hours Rapid within seconds

deficit maximum at onset

Transient ischemic

attacks (TIAs)

Absent Precedes stroke Precedes stroke

Vomiting Recurrent Absent or occasional Absent or occasional

Headache Severe and prominent Mild or absent Mild or absent

Early resolution

(within minutes or

days)

Unusual Variable Possible

Meningeal irritation May be present Absent Absent

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

Carotid bruit and

absence of pulse

Not observed Highly supports the diagnosis Possible

Valvular heart disease

and atrial fibrillation

Not found Unusual Highly supports the

diagnosis

CT scan findings Hemorrhage Early stage: Normal

Later: Pale infarct

Early stage: Normal

Later: Pale infarct

Localization of Stroke

Site of lesion Predominant clinical features

Cortex

Monoplegia common (brachial-MCA territory; crural-ACA territory)

Hemiplegia (may be present but never dense)

Contralateral 7th cranial nerve palsy (UMN variant)

Seizures

Aphasias (in dominant hemisphere)

Apraxias (in nondominant hemisphere)

Subcortical

(usually

secondary to

hypoperfusion)

Monoplegias common

Transcortical aphasias common

Internal capsule

lesion

Contralateral hemiplegia (dense)

Contralateral hemisensory loss

7th cranial nerve palsy (UMN variant)

Homonymous hemianopia

Broca’s like aphasia (only site to have subcortical aphasia).

Note: Most common etiology being ischemic and hence is territory specific. Since different parts of internal

capsule has blood supply from different blood vessels, all the above-mentioned features may not be present

at same time. However, if present, it suggests hemorrhage or tumor compressing internal capsule

Brainstem lesion Discussed in separate table

High cervical

cord lesion

(Brown-Sequard

syndrome)

Ipsilateral hemiplegia

Ipsilateral loss of posterior column sensation

Contralateral loss of pain and temperature sensation

Usually no cranial nerve involvement

(ACA: anterior cerebral artery; MCA: middle cerebral artery; UMN: upper motor neuron)

Fig. 6E.1: Localization of hemiplegia.

(UMN: upper motor neuron; LMN: lower motor neuron; MLF: medial longitudinal fasciculus)

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

•

Middle cerebral artery lesions and clinical features

Internal carotid artery M1 branch of MCA Stem of

MCA

M2 branches

of MCA

Both anterior cerebral artery (ACA) and middle

cerebral artery (MCA) territory involved along with

ophthalmic artery causing amaurosis fugax

Global aphasia

Dense hemiplegia (as internal capsule is

also involved due to involvement of

lenticulostriate branches of MCA)

Global

aphasia

Internal

capsule

spared

Superior

division

Inferior

division

(differences

described

below)

M2 stroke

Division of M2 Superior division Inferior division

Motor involvement Face, arm > leg Nil

Sensory Face, arm Nil

Vision Nil Quadrantanopia

Language Broca’s aphasia Wernicke’s aphasia

Nondominant Hemineglect Constructional apraxia

Brainstem syndromes

Site of

lesion/syndrome

Blood supply and tracts involved Ipsilateral features Contralateral

features

Midbrain

Benedict’s

syndrome

(Claude’s + Weber)

Interpeduncular branches of basilar artery, PCA—

posterior cerebral artery (midbrain tegmentum—CN

III fibers; red nucleus; CST; SCP)

Ipsilateral CN III palsy Ataxia +

Hyperkinesia

and tremor

(“rubral

tremor”) +

Hemiparesis

Claude’s

syndrome

PCA (midbrain tegmentum—CN III fibers; red

nucleus; SCP)

Ipsilateral CN III palsy Ataxia +

Tremor

(“rubral

tremor”)

Weber’s

syndrome

Paramedian branches of the basilar artery, PCA Ipsilateral CN III palsy Hemiparesis

Nothnagel

syndrome

Basilar penetrating artery, mesencephalic artery

(midbrain tectum Ipsilateral or bilateral CN III)

Oculomotor palsies; ataxia

Parinaud

syndrome

Midbrain dorsum (quadrigeminal plate region;

pretectum; periaqueductal gray matter)

Impaired upgaze; convergence

retraction nystagmus; dilated pupils

with light near dissociation

Top of basilar

artery syndrome

Midbrain

Thalamus

Portion of temporal and occipital lobe involved

Behavioral abnormalities

Ocular finding

Visual defects

Pupillary abnormalities

Motor deficits

Artery of

Percheron

stroke

Single thalamic perforating artery from the proximal

PCA

Altered sensorium

Vertical gaze palsy

Memory impairment

Pons

Raymond

Ceston

Long circumferential branch of basilar artery (CN VI;

CST)

6th nerve palsy Hemiparesis

•

•

•

•

•

•

•

•

•

•

•

•

syndrome

Millard-Gubler

syndrome

Basilar artery

(CN VII; CST)

7th nerve palsy

(± Lateral rectus palsy)

Hemiparesis

Foville’s

syndrome

Basilar artery

(CN VII; lateral gaze center, CST)

7th nerve palsy

+

Horizontal gaze palsy

Hemiparesis

Pierre-MarieFoix syndrome

AICA 6th + 7th nerve palsy

Horner’s syndrome

Hemiparesis

Medulla

Wallenberg

syndrome

(lateral medullary

syndrome)

Vertebral artery > PICA (Lateral medullary

Tegmentum—spinal tract of CN V and its nucleus;

nucleus ambiguus; emerging fibers of CNs IX and X;

LST; descending sympathetic fibers; vestibular

nuclei; inferior cerebellar peduncle; afferent

spinocerebellar tracts; lateral cuneate nucleus)

Loss of pain and temperature of

face

Ipsilateral decreased corneal reflex

Ipsilateral weakness of soft palate

Ipsilateral loss of gag reflex

Ipsilateral paralysis of vocal cord

Ipsilateral central Horner’s

syndrome

Nystagmus

Cerebellar ataxia of Ipsilateral limbs

Lateropulsion

Hiccups

Loss of pain

and

temperature

of body

Dejerine

syndrome

(medial medullary

syndrome)

Vertebral > anterior spinal artery Ipsilateral tongue weakness Hemiparesis

Avellis’

syndrome

Medullary tegmentum Ipsilateral palatal and vocal cord

weakness;

Loss of pain

and

temperature

Jackson’s

syndrome

Medullary tegmentum Ipsilateral flaccid paralysis of soft

palate, pharynx, and larynx; flaccid

weakness and atrophy of SCM and

trapezius (partial), and of the tongue

Schmidt’s Lower medullary tegmentum Ipsilateral paralysis of soft palate,

pharynx, and larynx; flaccid weakness

and atrophy of SCM and trapezius

(partial)

Céstan-Chenais Due to vertebral artery occlusion below origin of the

PICA; (nucleus ambiguus; ICP; sympathetics; CST;

ML)

Ipsilateral weakness of soft palate,

pharynx, and larynx; cerebellar ataxia;

Horner’s syndrome

Contralateral

hemiparesis

with loss of

posterior

column

function

Internuclear

ophthalmoplegia

(INO)

MLF lesion in the midbrain Ipsilateral adduction palsy Contralateral

gaze evoked

nystagmus

Wall eyed

bilateral

internuclear

ophthalmoplegia

(WEBINO)

Bilateral MLF lesion in the brain Bilateral adduction deficit and primary gaze position

exotropia

PCA syndromes

Gerstmann

syndrome

Parietal lobe Inability to write (dysgraphia or agraphia), the loss of

the ability to do mathematics (acalculia), the inability

to identify one’s own or another’s fingers (finger

•

•

•

•

•

•

•