agnosia), and inability to make the distinction between

the right and left side of the body.

Anton syndrome Bilateral occipital cortex involvement due to bilateral

PCA infarct

Anton’s syndrome describes the

condition in which patients deny their

blindness despite objective evidence

of visual loss, and moreover

confabulate to support their stance

Anosognosia

(or lack of

awareness of

defect) and

confabulation

Balint syndrome Parieto-occipital lobes on both sides of the brain Inability to perceive the visual field as a whole

(simultanagnosia), difficulty in fixating the eyes

(oculomotor apraxia), and inability to move the hand

to a specific object by using vision (optic ataxia)

(CN: cranial nerve; CST: corticospinal tract; SCP: superior cerebellar peduncle; AICA: anterior inferior

cerebellar artery; PICA: posterior inferior cerebellar artery; LST: lateral spinothalamic tract ; SCM:

sternocleidomastoid muscle; ICP: intracranial pressure; CST: corticospinal tract ; ML: medial leminiscus

; MLF: medial longitudinal fasciculus; PCA: posterior cerebral artery)

Transient Ischemic Attacks

Transient ischemic attack (TIA) is characterized by a brief episode of neurological dysfunction (sudden

loss of function) in which symptoms and signs resolve completely after a brief period within 24 hours

(usually within 30 minutes).

Transient ischemic attack is defined as a transient episode of neurologic dysfunction caused by focal

brain, spinal cord, or retinal ischemia, without acute infarction. However, TIAs may herald a stroke.

Newly proposed definition classifies those with new brain infarction as ischemic strokes regardless of

whether symptoms persist.

Clinical features: Hemiparesis and aphasia are most common. Other features include amaurosis fugax

(sudden transient loss of vision in one eye), hemisensory loss, hemianopic visual loss, diplopia, vertigo,

vomiting, choking and dysarthria, ataxia, etc.

Types of Transient Ischemic Attack

Large artery low-flow TIA—recurrent, short lasting episodes of stereotyped symptoms (shotgun

TIA/thrombotic TIA)

Embolic TIA—longer lasting less frequent episodes with varied symptoms, changing territories

Lacunar TIA.

Small Vessel (Lacunar) Stroke

Small penetrating arterial branches of 200–800 μm in diameter, supply the deep brain parenchyma.

Each of these small branches can be occluded either by atherothrombotic disease at its origin or by

the development of occlusive vasculopathy—lipohyalinotic thickening (consequence of hypertension)

(Table 6E.5).

Thrombosis of these vessels causes small infarcts that are referred to as lacunae. These infarcts

range in size from 0.2 mm to 15 mm in diameter.

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Fig. 6E.2: Cerebrovascular system (a comprehensive diagram of arterial system).

Fig. 6E.3: Blood supply of internal capsule.

(ACA: anterior cerebral artery; MCA: middle cerebral artery; PCA: posterior cerebral artery; AChA:

anterior choroidal artery; IC: internal carotid artery (direct branches); P. Comm: posterior communicating

artery)

Table 6E.5: Signs and symptoms of lacunar stroke depending on location of lesion.

Syndrome Signs/symptoms Localization Vascular supply

Pure motor Contralateral hemiparesis or

hemiplegia. Affects face, arm and leg

equally

Posterior limb of

internal capsule

Corona radiataBasis pontis

Lenticulostriate branches of the middle cerebral artery (MCA) or

perforating arteries from basilar

artery

Pure sensory Contralateral hemisensory loss.

Persistent or transient numbness

and/or tingling on one side of the body

Ventral

posterolateral

(VPL) nucleus

of thalamus

Lenticulostriate branches of MCA.

Small thalamoperforators of

posterior cerebral artery (PCA)

Mixed sensorimotor Contralateral weakness and numbness. Thalamus and Lenticulostriate branches of MCA

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Hemiparesis or hemiplegia with

ipsilateral sensory impairment

adjacent posterior

limb of internal

capsule

Dysarthria-clumsy hand Slurred speech and weakness of

contralateral hand (fine motor)

Basis pontis Basilar artery perforators

Ataxic-hemiparesis Combination of cerebellar and motor

symptoms. Contralateral hemiparesis

and ataxia out of proportion to

weakness

Internal

capsuleposterior limb

Basis pontis

Corona radiata

Lenticulostriate branches of

MCA

Perforating arteries of basilar

artery

Hemiballismus/hemichorea Contralesional limb flailing/dyskinesis Subthalamic

nucleus

Perforating arteries of anterior

choroidal or posterior

communicating artery (PCOM)

2. APPROACH TO SPINAL CORD DISEASES

Spinal Cord Anatomy

The spinal cord originates at the medulla and continues caudally to terminate at the filum terminale, a

fibrous extension of the conus medullaris is that terminates at the coccyx.

The adult spinal cord is approximately 45 cm long, oval or round in shape, and enlarged in the

cervical and lumbar regions, where neurons that innervative the upper and lower extremities,

respectively are located. The meninges that cover the spinal cord are continuous with those of the

brainstem and cerebral hemispheres.

Fig. 6E.4: Tracts of spinal cord.

The adult cord consists of 31 segments, each containing an exiting ventral motor root and entering

dorsal sensory root.

During embryologic development, growth of the cord lags behind that of the vertebral column, and in

the adult spinal cord ends at approximately the first lumbar vertebral body. The lower spinal nerves

take an increasingly downward course to exit via the appropriate intervertebral foramina.

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The first seven pairs of cervical spinal nerves exit above the same-numbered vertebral bodies,

whereas all the subsequent nerves exit below the same-numbered vertebral bodies; this situation is

due to the presence of eight cervical spinal cord segments but only seven cervical vertebrae.

The approximate relationship between spinal cord segments and the corresponding vertebral bodies

is shown in the following table:

Spinal cord level Corresponding vertebral body

Upper cervical

Lower cervical

Upper thoracic

Lower thoracic

Lumbar

Sacral

Coccygeal

Same as cord level

1 level higher

2 levels higher

2 to 3 levels higher

T 10 to T11

T12 to L1

L1

Features Suggestive of Involvement of Spinal Cord

Presence of sensory deficit and/or motor weakness in both lower limbs and/or upper limbs.

Bladder and bowel involvement

Brown-Sequard type of clinical picture

Presence of definite sensory level

Vertebral pain.

VASCULAR SUPPLY OF SPINAL CORD (FIG. 6E.5)

The anterior spinal artery: Union of the anterior spinal branches of the vertebral artery and

descends within the anterior median fissure.

The two posterior spinal arteries: Originate from the vertebral arteries and descend in the

posterolateral sulcus.

By themselves not sufficient and depend on feeder arteries that join them along their course (6–10

join the ASA and 10–20 join the PSA).

Thirty-one pairs of small radicular arteries: Supply corresponding nerve roots.

Some of them give a branch to spinal arteries: The radiculospinal branches.

C1-4: Vertebral artery.

C5-T2: Ascending and deep cervical artery.

T3 to T8: Intercostal artery.

T9 and below: Artery of Adamkiewicz—supplies most of the lower one-third of spinal cord; arises

from a left-sided intercostal or lumbar artery (T8-L3).

Fig. 6E.5: Vascular supply of spinal cord.

DIFFERENTIATION BETWEEN COMPRESSIVE AND NONCOMPRESSIVE

MYELOPATHY

Features Compressive Noncompressive

Bony deformity + –

Bony tenderness + –

Girdle like sensation + –

Upper level of sensory loss + –

Zone of hyperesthesia + –

Root pain + –

Onset and progress Gradual May be acute

Symmetry Asymmetrical Majority are symmetrical

Flexor spasm Common Usually absent

Pattern of neurodeficit U-shaped (Ellsberg phenomenon) Bilaterally symmetrical

Bladder and bowel movement Late Early (acute transverse myelitis)

Selective tract involvement Rare Usually seen

Flowchart 6E.3 depicts the types of spinal cord diseases.

Compressive myelopathies examples

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Trauma

Tumor

Tuberculosis

Myeloma

Metastasis

Extramedullary extradural

Caries spine

Metastasis

Intervertebral disc prolapse

Spondylosis

Fluorosis

Trauma to vertebra

Epidural abscess

Epidural hematoma

Hematomyelia

Extramedullary intradural

Meningioma

Neurofibroma

Schwannoma

Patchy arachnoiditis

Arteriovenous malformations

Lipoma

Sarcoma

Dermoid

Intramedullary

Ependymoma

Chordoma

Glioma

Flowchart 6E.3: Types of spinal cord diseases.

Noncompressive myelopathies examples

Inflammatory

Infectious—viral, bacterial, fungal, and parasitic

Autoimmune—SLE, Sjogren’s, sarcoidosis, Bechet syndrome, MCTD, polyarteritis nodosa, pANCA positive vasculitis

Demyelinating—MS, NMO, ADEM, and postviral postvaccinial

Paraneoplastic—lung carcinoma, breast, and ovary

Encephalomyelitis

Noninflammatory

Inherited—HSP, inherited metabolic disorders

Metabolic—vitamin B12

, copper, folate and vitamin E deficiency—AIDS associated

Toxic—cassava, lathyrism, fluorosis, SMON, nitrous oxide, TOCP, and Konzo

Vascular—anterior spinal artery thrombosis, AVM, and dural arteriovenous fistula

Degenerative—familial spastic paraplegia

Physical agents—electrical injury, Caisson’s disease, and radiation myelopathy

(SLE: systemic lupus erythematosus; MCTD: mixed connective tissue disease; pANCA: perinuclear

antineutrophil cytoplasmic antibodies; MS: multiple sclerosis; NMO: neuromyelitis optica; ADEM: acute

disseminated encephalomyelitis; HSP: hereditary spastic paraplegia; AIDS: acquired immunodeficiency

syndrome; SMON: subacute myelo-optic neuropathy; TOCP: triorthocresyl phosphate; AVM:

arteriovenous malformation)

Discriminate Between Extramedullary and Intramedullary Lesions

Features Extramedullary Intramedullary

Radicular pain Common

Intradural: Unilateral

Extradural: Bilateral

Unusual

Vertebral pain Common (extradural) Unusual

Funicular pain Rare Common

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Motor deficit Ascending motor weakness, i.e. sacral →

lumbar → thoracic → cervical

Descending pattern of loss, i.e. cervical → thoracic → lumbar → sacral

Upper motor neuron

involvement

Early and prominent Less pronounced; late feature

Lower motor neuron

involvement

Segmental Marked with widespread atrophy, fasiculations seen

Reflexes Brisk early feature Less brisk, later feature

Sensory deficit Ascending sensory loss, i.e. sacral → lumbar → thoracic → cervical

Saddle anesthesia

Hemisection—contralateral loss of pain and

temperature, ipsilateral loss of joint position

Descending pattern of loss, i.e. cervical → thoracic → lumbar → sacral

Dissociative sensory loss

Suspended sensory loss (Jacket pattern)

Sacral sensation Lost (early) Sacral sparing

Autonomic

involvement (bladder

and bowel)

Late Early

Trophic changes Usually not marked Common

Vertebral tenderness May be present (extradural) No bony tenderness in vertebrae

Changes in CSF Frequent (increased protein, cells) Rare

Fig. 6E.6: Arrangement of motor fibers.

Fig. 6E.7: Bladder involvement in spinal cord

disease.

Differences Between Presentation of Intradural and Extradural Lesion

Features Extradural Intradural

Mode of onset Usually symmetrical Asymmetrical

Root pain Less common More common

Spinal tenderness Common Uncommon

Spinal deformity Present Absent

Patterns of Spinal Cord Disease

Complete cord transection syndrome

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