Lesions to Cerebral Cortex

• Brodmann’s Areas

Brodmann’s	Name	Result of Lesion
1,2,3	Primary somesthetic area	Contralateral impairment of touch, pressure, propioception
4	Primary motor cortex	Contralateral flaccid paralysis
6	Supplementary motor cortex	Spasticity, increased DTRs
8	Frontal eye fields	Loss of voluntary movement of eyes to contralateral field
17,18,19	Visual cortex	Contralateral visual field loss, visual agnosia
22	Wernicke’s area	Receptive aphasia (dominant hemisphere)
39	Angular gyrus	Alexia, agraphia, (dominant hemisphere)
40	Supramarginal gyrus	Tacticle/propioceptive agnosia, apraxia, left/right confusion (dominant hemisphere)
41,42	Auditory area	None (hearing is bilaterally represented)
44,45	Broca’s area	Expressive aphasia (dominant hemisphere)

• 95% of R-handed patients are L brain dominant
• 70% of L-handed patients are L brain dominant.  15% are R brain dominant and 15% have bilateral components.
• Frontal Lobe

• Nondominant:
• Contralateral spastic hemiplegia and ipsilateral gaze preference
• Slight elevation of mood, difficulty in adaptation, loss of initiative
• If entirely prefrontal – no hemiplegia but will see grasp/suck reflexes or instinctive grasping
• Aprosody (loss of speech intonation)
• Anosmia with involvement of orbital part
• Dominant – see all nondominant frontal abnormalities plus:
• Motor speech disorder with agraphia, with or without apraxia of lips and tongue
• Sympathetic apraxia of left hand
• Loss of verbal associative fluency, perseveration
• Bilateral:
• Bilateral hemiplegia
• Spastic bulbar (pseudobulbar) palsy
• If prefrontal – abulia or akinetic mutism; lack of ability to sustain attention or solve complex problems; rigidity of thinking; bland affect; social ineptitude; behavioral disinhibition; inability to anticipate; labile mood, grasping, sucking, decomposition of gait, and sphincter incontinence
• Temporal Lobe – can produce contralateral superior quadrantanopsia
• Nondominant
• Inability to judge spatial relationships in some cases
• Inability to form visual and auditory memory
• Impairment in tests of visually presented nonverbal material
• Agnosia for sounds and some qualities of music
• Dominant
• Wernicke’s aphasia
• Amnesia
• Dysnomia or amnestic aphasia
• Visual agnosia
• Impaired ability to form verbal memory and/or short term memory
• Either Lobe
• Homonymous upper quadrantanopsia
• Auditory, visual, olfactory, and gustatory hallucinations
• Dreamy states with uncinate seizures
• Emotional and behavioral changes
• Delirium (usually nondominant)
• Bilateral:
• Korsakoff amnestic deficit (hippocampal formation)
• Klüver-Bucy Synrdome
• Apathy and placidity
• Increased sexual activity
• Sham rage
• Parietal Lobe
• Unilateral
• Cortical sensory syndrome with sensory extinction (or total hemianesthesia with large acute lesions of white matter)
• Mild hemiparesis, unilateral muscular atrophy in children, hypotonia, poverty of movement, hemiataxia
• Homonymous hemianopsia or visual attention; sometimes anosognosia, neglect of one-half of body and of extrapersonal space (observed more frequently with right than with left parietal lesions)
• Abolition of optokinetic nystagmus with target moving toward side of lesion
• Dominant
• Disorders of language (esp. alexia and color dysnomia)
• Gersmann’s syndrome:
• Finger agnosia
• Left-right confusion
• Acalculia
• Agraphia
• Tactile agnosia (bilateral astereognosis)
• Bilateral ideomotor and ideational apraxia (cannot use comb or tool)
• Nondominant
• Visual/spatial disorder
• Topographic memory loss (constructional apraxia, dressing apraxia)
• Anosognosia and dressing apraxia (also may occur in dominant lesions), neglect, blunted emotion
• Confusion
• Tendency to keep eyes closed, resist opening, blepharospasm
• Bilateral
• Visual spatial imperception, optic ataxia, spatial disorientation, severe constructional apraxia
• Topognosia (inability to localize touch/pain stimuli)
• Occipital Lobe
• Unilateral
• Contralateral congruent homonymous hemianopsia; also homonymous hemiachromatopsia
• Elementary (unformed) hallucinations – due to irritative lesions
• Left
• In deep white matter or splenium – alexia and color-naming deficit, without agraphia (can see with right visual cortex but cannot transmit to left association area for interpretation)
• Right
• Loss of topographic memory and visual orientation
• Bilateral
• Cortical blindness (with reactive pupils)
• Anton syndrome (claim sight although blind)
• Achromatopsia (loss of perception of color)
• Prosopagnosia
• Simultanognosia
• Balint syndrome:
• Inability to look voluntarily into and scan peripheral field (psychic paresis of fixation of gaze)
• Optic apraxia – failure to touch or grasp object under visual guidance, as though hand and eye were not coordinated
• Visual inattention (disorientation) involving mainly peripheral field
• Parasagittal Lesions
• Paresis of lower extremities (typically beginning in one foot, spreading up leg, then involving other leg), focal motor/sensory seizures (involving LEs), incontinence of urine/stool, frontal lobe syndrome