disorders of higher function

Infarction

An area of tissue death due to lack of oxygen.

Ischemic vs. Hemorrhagic Stroke Percentage

Ischemic infarction causes ~85% of acute strokes; intracerebral/subarachnoid hemorrhage causes ~15%.

Leading Cause of Infarction

Cerebrovascular disease (80%) — hemodynamic/occlusive emboli (cardiogenic embolism causes 15%; dissections, hypercoagulable states, vasculitis, and systemic hypotension make up 5%).

Four Cardiogenic Causes of Embolism

Atrial fibrillation, ischemic heart disease, valvular heart disease, infective endocarditis.

3 Types of Ischemic Events

1) Transient Ischemic Attack (TIA), 2) Reversible Ischemic Neurological Deficit (RIND), 3) Cerebral Infarction.

Differentiating TIA, RIND, and Cerebral Infarction

TIA: temporary focal deficit, resolves in 2-15 min (up to 24 hrs), no permanent deficit. RIND: focal ischemia improving within ≤72 hours. Cerebral infarction: permanent disorder with fixed deficits.

Common Warning Symptoms of a TIA

Numb hand/arm or one side of face/tongue, loss of strength in arm/hand/leg, difficulty speaking or reading, amaurosis fugax.

Anterior Cerebral Artery (ACA) Supply

The medial surface of the frontal lobe, parietal lobe, and occipital lobe.

Middle Cerebral Artery (MCA) and Circle of Willis

The largest branch of the internal carotid artery; it is NOT part of the Circle of Willis.

Middle Cerebral Artery Supply

Anterior temporal lobes, parietal lobes, frontal lobes (and lateral frontal lobe).

Internal Carotid Artery Occlusion Presentation

Variable presentation: monoparesis to hemiparesis with or without a visual defect, transient monocular blindness, impaired speech/language.

Classic Initial Symptom of Internal Carotid Artery Dissection

Horner's syndrome, because post-ganglionic sympathetic fibers travel in close proximity to the ICA.

Symptoms Suggesting ICA Dissection Besides Horner's

Facial pain, neck pain, headache, contralateral sensorimotor deficit.

Suspected Condition in Young Patient with Stroke and Neck Trauma

Carotid (or vertebral) artery dissection.

Symptoms of Middle Cerebral Artery Occlusion

Hemiplegia of contralateral face and upper body, hemi-sensory defect, contralateral hemianopsia, aphasia if dominant hemisphere is affected.

Symptoms of Anterior Cerebral Artery Occlusion

Weakness and sensory loss of the opposite leg, gait apraxia, cognitive impairment.

Three Most Common Locations for a Cerebral Aneurysm

Anterior communicating artery, distal ICA, middle cerebral artery.

Prevalence of Unruptured Aneurysms by Sex

~5% in women, ~4% in men; most unruptured aneurysms are smaller than 12 mm.

Three Treatment Options for Aneurysms

Clipping, coiling, stenting (pipeline technology).

Basilar Artery Formation and Supply

The two vertebral arteries join to form the basilar artery; it supplies the base of the cerebrum and most of the cerebellum.

Basilar and Posterior Cerebral Artery (PCA) Supply

The occipital lobe, brainstem, optic radiations, and cerebellum.

Vertebro-Basilar System Overall Supply

The medulla, pons, midbrain, thalamus, cerebellum, and occipital cortex.

Hallmark Presentation of Vertebro-Basilar System Ischemia

Severe vertigo and nystagmus, plus nausea, vomiting, dysphagia, ipsilateral cerebellar ataxia, decreased pain/temperature discrimination, diplopia, visual field loss, and gaze palsies.

Two Hallmark Findings of Vertebro-Basilar Disease

Vertigo/dizziness and nystagmus.

Most Common Cause of Vertebro-Basilar Disease

Atherosclerosis at the origin of the vertebral artery at the subclavian region.

Vertebral vs. Carotid Artery Dissection Frequency

Carotid dissection occurs at 2.5-3/100,000; vertebral at 1-1.5/100,000.

Causes of Vertebral Artery Dissection

Spontaneous (head movement), chiropractic manipulation, 'beauty shop dolichoectasia', stargazing.

'Beauty Shop Dolichoectasia'

Vertebral artery injury/compromise from prolonged neck hyperextension over a salon sink, causing posterior circulation ischemic symptoms.

Vertebral Artery Dolichoectasia

An elongated, distended, or tortuous vertebral artery that may compress cranial nerves.

Characteristic Presentation of Vertebro-Basilar Artery Disease

Sudden hearing loss and vertigo lasting a few minutes with nausea and vomiting.

Three Major Cerebellar Arteries

SCA (superior cerebellar artery), AICA (anterior inferior cerebellar artery), PICA (posterior inferior cerebellar artery).

Visual Disturbances Typical of Vertebro-Basilar Disease

Diplopia, blurry vision, positive visual phenomena, transient achromatopsia, oropharyngeal dysfunction.

'Drop Attack' in Posterior Circulation TIA

A sudden decrease in blood supply to the posterior circulation causing gait disturbance and limb weakness/ataxia.

TRIAD of Vertebro-Basilar Insufficiency

Dimming or blurry vision in both eyes, headache, dizziness (typically in older patients).

Differentiating Vertebro-Basilar Insufficiency from Migraine

By age of onset and family history/previous episodes of migraine.

Four Syndromes of Vertebro-Basilar Disease

Subclavian steal syndrome, midbrain syndromes, pontine syndromes, medullary syndromes.

Subclavian Steal Syndrome

Subclavian artery stenosis causes retrograde blood flow from the basilar artery down the ipsilateral vertebral artery to supply the arm, 'stealing' brainstem blood flow.

Symptoms of Subclavian Steal Syndrome

Vertigo, syncope, dysarthria, nystagmus, diplopia, visual field defects.

Hallmark Ocular Signs of a Midbrain Lesion

Supranuclear CN III palsy and vertical gaze palsy; patients are often somnolent or ataxic.

Top-of-the-Basilar Syndrome Causes

Infarcts from posterior circulation emboli, dissection, or systemic hypotension.

Dorsal Midbrain (Parinaud's) Syndrome Features

Impaired up-gaze, unresponsive pupils, light-near dissociation, bilateral lid retraction, skew deviation, convergence-retraction nystagmus, CN IV palsy, preserved VOR.

Weber Syndrome

A ventral midbrain syndrome: ipsilateral CN III palsy + contralateral hemiparesis.

Benedikt Syndrome

A ventral midbrain syndrome: ipsilateral CN III palsy + contralateral hemi-tremor/ataxia.

Difference Between Weber and Benedikt Syndromes

Both have ipsilateral CN III palsy; Weber has contralateral hemiparesis, while Benedikt has contralateral hemi-tremor/ataxia.

Hallmark Ocular Signs of Pontine Syndromes

CN VI and CN VII palsy, horizontal gaze palsy, ocular bobbing.

Locked-In Syndrome

Full paralysis with preserved consciousness; patient communicates by blinking and eye movement.

INO (Internuclear Ophthalmoplegia)

MLF lesion between CN III and CN VI causing no adduction on the ipsilateral side with normal abduction of the contralateral eye.

WEBINO (Wall-Eyed Bilateral INO)

Bilateral INO with bilateral adduction deficit producing an exotropic appearance.

One-and-a-Half Syndrome

Combination of INO plus ipsilateral horizontal gaze palsy from MLF and PPRF lesions.

Millard-Gubler Syndrome

A ventral pontine syndrome: CN VI palsy, CN VII palsy, and contralateral hemiparesis.

Foville Syndrome

A lower dorsal pontine syndrome: ipsilateral CN V, VII, VIII palsy, Horner's syndrome, and horizontal conjugate gaze palsy.

Hallmark Signs of Medullary Syndromes

Ischemic etiology, Horner's syndrome, ipsilateral facial pain and temperature loss, ipsilateral paralysis of the tongue, soft palate, and vocal cord.

Lateral Medullary (Wallenberg) Syndrome

Caused by PICA occlusion; features reduced corneal reflex, vertigo/nausea/vomiting, and ocular lateropulsion.

Posterior Cerebral Artery (PCA) Occlusion Causes

Cortical blindness, contralateral hemianopia with macular sparing, color blindness, failure to see movement, verbal dyslexia, hallucinations.

Subarachnoid Hemorrhage

Blood in the subarachnoid space of the brain and spinal cord.

Causes of Hemorrhagic Events

Trauma, ruptured intracranial aneurysms, arteriovenous malformation, vasculitis, tumor, anticoagulants, coagulation disorders.

Risk Factors for Hemorrhagic Stroke

Hypertension, smoking, alcohol consumption, pregnancy/straining, drug abuse (e.g., cocaine).

Classic Presentation of a Ruptured Aneurysm

'Worst headache of my life,' nausea and vomiting, nuchal rigidity, photophobia, diplopia, seizures.

Complications of Subarachnoid Hemorrhage

Re-bleeding, hydrocephalus, delayed cerebral ischemia.

Main Treatment Strategies for Ischemic Stroke

Control risk factors, surgical intervention, acute anticoagulants, chronic antiplatelet agents.

Ganglion Cell Pathways in Primate Vision

3 pathways: Parvocellular, Magnocellular, Koniocellular.

Parvocellular Pathway

Uses midget ganglion cells for fine spatial resolution and red-green color opponency; static firing system.

Magnocellular Pathway

Uses parasol ganglion cells for motion information; phasic firing system.

Koniocellular Pathway

Uses bistratified ganglion cells for blue-yellow color opponency.

Two Occipitofugal Pathways and Functions

Dorsal ('Where?') pathway for visuospatial analysis/localization; Ventral ('What?') pathway for object identification/recognition.

Dorsal ('Where?') Pathway Trace

V1 → V2 → V3 → V5 → parietal and superior temporal cortex.

Lesions of the Dorsal Occipitofugal Pathway

Cause hemi-spatial neglect and Balint's syndrome.

Simultanagnosia

Inability to integrate multiple elements of a scene into a global image from posterior parietal cortex lesions.

Optic Ataxia

Visual input disconnected from the motor system; patient reaches for an object as if blind.

Spasm of Fixation

Loss of voluntary eye movement with persistent fixation from frontal eye field damage.

Hemi-Spatial Neglect

Inability to attend to stimuli in the left visual field caused by right hemisphere damage.

Visual Allesthesia

Retinotopic visual field rotated, flipped, or inverted from medulla or posterior parietal cortex lesions.

Ventral ('What?') Pathway Trace

V1 → V2/V4 → inferior temporal cortical areas, angular gyrus, and limbic structures.

Lesions of the Ventral Occipitofugal Pathway

Cause visual alexia, anomia, visual agnosia, visual amnesia, and visual hypo-emotionality.

'Visual-Verbal Disconnection' Syndrome

Caused by left occipital lobe infarctions; produces difficulty naming objects from sight, alexia without agraphia, color anomia, and optic anomia.

Prosopagnosia

Loss of identification of familiar faces from bilateral occipito-temporal cortex damage.

Associative Object Agnosia

Loss of object identification from bilateral occipito-temporal cortex damage.

Cortical Areas V1-V5 Locations and Functions

V1=striate cortex; V2-V3=surround striate; V4=ventromedial occipital (color); V5=lateral occipital (motion).

Anton's Syndrome

Bilateral striate cortex damage causing denial of blindness.

Blindsight

Unconscious, basic visual perception persisting in blind patients after visual cortex lesions.

Riddoch's Phenomenon (Statokinetic Dissociation)

Preservation of motion perception in an otherwise blind hemifield; recovery indicator.

Cerebral Achromatopsia

Damage to the ventro-medial occipital cortex (V4); causes color vision loss.

Akinetopsia

Loss of visual motion perception with preserved form, texture, and color vision from V5 damage.

Charles Bonnet Syndrome

Release hallucination in bilateral visual loss patients with normal psychiatric status.

Palinopsia

Pathological persistence of a previously seen image, usually associated with a homonymous visual field defect.

Cerebral Polyopia

Seeing two or more images of a single object, often with homonymous field defects.