Neurology For Pep

Front 1

primary auditory cortex

Back 1

Superior temporal gyrus in both temporal lobes. Thalamus is a relay station for much of the sensory input.

Front 2

upper motor neuron lesion signs

Back 2

spasticity, muscle weakness, exaggerated reflexes, extensor plantar response (Babinski)

Front 3

lower motor neuron lesion signs

Back 3

fasciculations, paralysis, weakening of muscles, atrophy, hyporeflexia

Front 4

Papez circuit

Back 4

one of the major pathways of the limbic system and is chiefly involved in the cortical control of emotion. The Papez circuit plays a role in storing memory.


Hippocampal formation (Subiculum) → fornix → mammillary bodies
Mammillary bodies → mammillothalamic tract → anterior thalamic nucleus
Anterior thalamic nucleus → genu of the internal capsule → cingulate gyrus
Cingulate gyrus → cingulum → parahippocampal gyrus
Parahippocampal gyrus → entorhinal cortex → perforant pathway → hippocampus

Front 5

What are Argyll Robertson pupils, and what are they characteristic of

Back 5

Small, irregular pupils that constrict to accomodation but not to light. They are characteristic of late stage syphillis.

Front 6

Klüver-Bucy Syndrome

Back 6

Clinical features: hypersexuality, placidity, hyperorality. Results from bilateral destruction of amygdaloid bodies, and inferior temporal cortex. Can be caused by Pick's Disease, also by stroke and Alzheimer's

Front 7

Prosopagnosia

Back 7

Inability to recognize faces

Front 8

Pick's disease

Back 8

Pick’s disease, also known as Pick disease and PiD, is a rare neurodegenerative disease. Pick's disease (the pathology) causes progressive destruction of nerve cells in the brain and causes tau proteins to accumulate into "Pick bodies"[1] that are a defining characteristic of the disease. Pick's disease is one of the causes of the clinical syndrome of frontotemporal lobar degeneration which has three subtypes. Pick's disease pathology is associated more with the frontotemporal dementia and progressive nonfluent aphasia subtypes than the semantic dementia subtype.

Front 9

cataplexy

Back 9

An individual suddenly feels weak and collapses at times of strong emotion such as during laughter, anger, fear, or surprise. In so collapsing, people with cataplexy may injure themselves. Cataplexy often affects people who have narcolepsy.

Front 10

Catalepsy

Back 10

A body's persistence in unusual postures, with waxy rigidity of the limbs, mutism, and complete inactivity, regardless of outside stimuli, as is sometimes seen in catatonic schizophrenia.

Front 11

Broca's aphasia

Back 11

broken, stuttering, staccato speech, with inability to repeat, phonemic and paraphrasic errors. Auditory comprehension is intact. The result of a lesion in the left, posterior inferior frontal gyrus.

Front 12

Wernicke's aphasia

Back 12

speech is fluent, comprehension is impaired. Speech is logorrheic (overproductive) with neologisms, paraphrasic errors. Results from a lesion in the superior temporal gyrus.

Front 13

conduction aphasia

Back 13

Marked by the inability to repeat, but generally intact comprehension, and relatively normal spontaneous speech although with some paraphrasic errors and hesitancy. Lesion usually in the inferior parietal or superior temporal regions.

Front 14

global aphasia

Back 14

Speech is nonfluent or mute, comprehension is impaired. Naming, repeating, writing and reading are all impaired. Results from large lesions in the superior temporal, inferior frontal and parietal lobes. Region generally corresponds to the middle cerebral artery.

Front 15

Anton's Syndrome

Back 15

An agnosia characterized by cortical blindness. Lesion in bilateral occipital lobes, usually due to strokes. Region associated with bilateral posterior cerebral arteries.

Front 16

pontine myelinolysis

Back 16

The classic complication of rapid sodium replacement in hyponatremia. This can result in clinical transection of the pons and lead to a locked in syndrome.

Front 17

normal pressure hydrocephalus symptoms

Back 17

dementia, incontinence, gait disturbance

Front 18

cortical vs subcortical dementia

Back 18

Cortical dementias (e.g. Alzheimer's) show gradual cognitive decline with normal speed of cognition, aphasia, dyspraxia and agnosia. Depression is less common. Motor abnrmalities are usually absent unless in terminal stages. Subcortical (e.g. Parkinson's) usually present with dysarthria, EPS. Apathy and depression often present. Frontal memory impairment (aided with cues) often noted. Speed of cognition is slow.