Neuro Block 3-Pt-4

ptheodore's version from 2015-08-03 01:39

Brodmann’s Areas

Question Answer
44, 45Broca’s area
22Wernicke’s area
22, 39 and 40 Wernicke’s area
8Frontal eye field
4Primary motor gyrus
1,2,3Primary sensory gyrus
17Primary visual fields
9-12, 46, 47 Prefrontal cortex
5, 7 Somatosensory association cortex (upper part of parietal lobe)
20, 21, 22 Inferior, middle, superior temporal gyri
23, 24, 29-33Cingulate gyrus
18, 19Associations visual areas
41, 42primary auditory
6Supplementary motor area
28 and 34.Entorhinal cortex

Layers of the Cortex

Question Answer
Molecular Layer1
External granular layer2
External pyramidal layer3
Internal granular layer4
Ganglionic layer (internal pyramidal layer)5
Multiform layer (layer of polymorphic cells)6
What kind of cells are found in the granular layersStellate cells
What kind of cells are found in the superficial layersHorizontal (intracortical cells) (of Cajal)
What kind of cells are found in the deep layersFusiform cells
Betz cellsHuge pyramidal cells
Big betz cells are ONLY found in theMotor cortex
Main interneuron of the cortex. Stellate (granule) cells
Receives ARAS. Non specific afferents from intralaminar nucleus of thalamus and brainstem areas.Molecular layer (I)
Receives corpus callosum (callosal) and association afferents.External granule layer (II)
Association and commissural fibers originate here.External pyramidal layer (III)
Receives afferents from thalamic nuclei, ie. this is the termination point of thalamic relay neurons (specifically VPL and VPM for post central gyrus, LGN for visual cortex).Internal granule layer (IV)
Origin of motor tracts (corticospinal, corticobulbar, and corticostriatal fibers)Internal pyramidal layer (V)/Ganglionic Layer
Also gives rise to association and commissural fibers; most corticothalamic.Multiform layer (VI)
Granular layers (2, 4) are very big, but pyramidal layers (3, 5) are not. This is the typical arrangement in major sensory areas (like postcentral gyrus).Granular
Pyramidal layers (3, 5) are very big, but granular layers (2, 4) are not. Obvious example is precentral gyrus.Agranular
The Columns of the coxted are linked viahorizontal (intracortical) cells


Question Answer
Akinetic mutism (patients don’t tend to move or speak) or tactile agnosia (can’t recognize objects by touch).Genu (Anterior) of Corpus Callosum
Alexia without agraphia (can’t read but can write)Splenium (Posterior) of Corpus Callosum
Genu of corpus callosum also known asForceps Minor
Splenium of corpus callosum also known asForceps Major.
Connects the pretectal nuclei (tectum), for pupillary light reflex.Posterior commissure
Lesion results in loss of consensual, BUT NOT direct, light response.Posterior commissure
Connects the hippocampus with contralateral mammillary body.Fornix
Some olfactory axons cross here, also some spinothalamic axons.Anterior commissure
Connects frontal, parietal, and occipital lobes.Superior longitudinal fasciculus
Connect Wernicke's and broca's.Arcuate fasciculus
Connects cingulate gyrus to other limbic structures. Cingulum
Connect nearby gyri.Arcuate fibers
Fibers if going from the cortex (motor).Corticofugal
Fibers if going to the cortex (sensory).Corticopetal
Corticobulbar (genu) and Corticospinal go through what part of the internal capsuleThe posterior limb
Corticostriate and corticopontine go through what part of the internal capsuleAnterior limb
Corticofugal for extrapyramidal tracts goes through what part of the internal capsulePosterior limb
3rd order neurons from VPL and VPM of thalamus go through what part of the internal capsule on their way to the cortex.Posterior limb
PaleocortexOlfactory system
ArchicortexHippocampus and related structures
Neocortex A.K.ACerebral Cortex
Executive function regulates and directs cognitive processes such as decision making, problem solving, learning, reasoning and strategic thinking.The prefrontal cortex (Executive functions)
Personality changes, Deficits in strategic planning, Perseveration (doing the same thing over and over), Release of ‘primitive (baby)’ reflexes, Abulia (Loss of desire/ability to perform voluntary actions), Sphincteric incontinence.Frontal Lobe Syndrome
Inferior surface of frontal lobe. Limbic connections, for social behavior.Orbitofrontal (prefrontal cortex)
Middle and superior frontal gyri. Concentration, planning, judgment, problem solving, etc.Dorsolateral (prefrontal cortex)
Contralateral paralysis, hyperreflexia, Babinski...Primary Motor Cortex (4)
Involved in planning of movement, i.e. ‘integration of sensory and motor information for the performance of an action’.Premotor Cortex (6)
Damage symptoms can vary, but might include Alien Hand Syndrome.Supplementary motor area (anteromedial part of Premotor Cortex)
Ask the patient to put their arms out straight, supinated. (Eyes closed). The affected arm will slowly pronate and ‘drift’ away.Pronator drift is another (Symptoms of lateral corticospinal tract damage/UMN test)
Damage on one side; hemianopia with macular sparing. Area 17
Secondary and tertiary visual cortices also known as visual association cortex. Possible visual hallucinations.Areas 18, 19
Damage to area 39 (Angular gyrus) and often area 40 as well (supramarginal gyrus). Dominant hemisphere only.Gerstmann’s Syndrome
Contralateral hemi- or quadrantinopia (hit cranial 2, while it’s heading to area 17), Right-left confusion, Finger agnosia (can’t differentiate fingers), Agraphia (Can’t write), Dyscalculia (Can’t understand Numbers)Gerstmann’s Syndrome
Unilateral lesion results in maybe a little hearing loss, bilateral = cortical deafness.41/42 (Primary auditory)
Contralateral upper quandrantinopia (‘pie in the sky’).Meyer’s loop
Ipsilateral anosmia (loss of smell)Primary olfactory cortex (34)
Apraxia, Aphasia, Agraphia, Gerstmann’s SyndromeDominant Hemisphere
Dysprosody, Anosognosia, Constructional apraxia, dressing apraxiaNon-Dominant hemisphere
Astereognosis, NeglectEither Hemisphere
Prosopagnosia, Balint’s SyndromeBoth Hemispheres
Degeneration of ACh neurons in the nucleus basalis of Meynert (forebrain). Neuro-degenerative disorder (irreversible and progressive).Alzheimer’s
Hirano bodies – the inclusion bodiesAlzheimer’s
Loss of ACh neurons in nucleus basalis. Beta-amyloid plaque accumulation. Neurofibrillary tangles. Tau proteinAlzheimer’s
Patient is confused, forgetfulness, disorientation, anger, apprehensiveAlzheimer’s
Age related ischemic damage to white matter results in an Alzheimer’s like dementia. Follows hypertension or other vascular problemsBinswanger’s subcortical leukoencephalopathy


Question Answer
Loss of ability to comprehend written/spoken language. Can’t Write. Have BAD comprehension, GOOD production (DON’T MAKE SENSE), poor repetitionReceptive (Wernicke’s) Aphasia A.K.A Fluent or Sensory
Inability to transform thoughts into words (loss of speech production). Have good comprehension, poor speech production, poor repetitionExpressive (Broca’s) Aphasia A.K.A Motor or Non-Fluent
Wernicke’s can occur, and Broca’s patients typically have contralateral lower face and arm weakness due to which arteryLeft M3 of MCA
Lesion of the arcuate fasciculus.Conduction Aphasia
Patient can speak and understand, but can’t repeat wordsLesion of the arcuate fasciculus (Conduction Aphasia)
Connects Wernicke’s to motor and premotor areas of the frontal cortexArcuate fasciculus
Results in loss of comprehension, or use, of inflection/emotional content in speech. Lesion of Wernicke’s and Broca’s areas in the non-dominant hemisphere
Receptive and Expressive Dysprosody, respectivelyLesion of Wernicke’s and Broca’s areas in the non-dominant hemisphere
Area near Broca’s (watershed) is damaged, but not Broca’s. Patient has great difficulty producing speech, but has no problem repeating (arcuate fasciculus is still intact). Comprehension, reading, naming are good.Transcortical motor aphasia
Damage near Wernicke’s area. Naming, reading, comprehension are poor, but speech fluent and grammatical. Repetition is good. Patient tends to substitute ‘similar’ words often (like pencil for pen, or apple for orange). Transcortical sensory aphasia
Poor comprehension, poor speech production from damage to both Wernicke’s and Broca’s areas. May include conduction aphasia deficits. Most severe aphasia, also known as Mixed Transcortical Aphasia. Global aphasia
Inability to recognize the presence of disease in one’s self (Alzheimer's patients).Anosognosia
Inability to recognize a part of the body.Autotopagnosia
Inability to recognize spatial positioning of body parts.Statognosis
Loss of ability to determine an object’s form by touching it with Either handsTactile agnosia/amnesia
Loss of ability to determine an object’s form by touching it with BOTH handsAstereognosis
Inability to recognize speech, animal sounds, mechanical sounds.Auditory agnosia
Inability to recognize facesProsopagnosia
Cannot recognize figures (numbers) drawn on their skin.Graphesthesia
Following a hemispheric lesion, the person is unable to perceive stimuli from the contralateral environment or body. Usually in the PARIETAL LOBENeglect
Cannot reproduce the drawing properly, but gets most of itConstructional Apraxia
Copies the drawing accurately, but only one side.Neglect
Cannot reproduce the drawing, and ignores one half of it.Constructional apraxia with neglect
A term specific for not perceiving one side of the body. Patient is usually indifferent about the ‘missing’ limb (“I dunno where my left arm is, what’s for dinner?”).Asomatognosia
The patient shows ‘delusional’ misidentification, or confabulation, with regards to the affected limb (“That’s not my arm, that’s the doctor’s arm”, or “That’s not my arm, but she’s wearing my ring”).Somatoparaphrenia
Inability to correctly imitate hand gestures and voluntarily ‘pantomime’ tool use, i.e. pretend to brush one's hair when asked. (But spontaneous brushing may occur). Damage to Dominant parietal lobe.Ideomotor apraxia
Inability to correctly perform a series of movements to accomplish a task (putting on shoes and socks). Items may be used incorrectly (brushing hair with a pen). Damage to Dominant parietal lobe.Ideational apraxia
Inability to perform facial or oral motor acts on command (ie. licking lips). Dominant parietal lobe.Facial apraxia
Inability to draw simple objects. Non dominant parietal lobe.Constructional apraxia
Inability to dress (button shirt, etc). Often associated with neglect. Non dominant parietal lobe.Dressing apraxia
Inability to voluntarily open the eyes. (non-dominant parietal or frontal lobe).Lid opening apraxia
Inability to execute voluntary movements in response to visual stimuli. Individual has normal visual fields and acuity, but will fixate on only one object, and is unable to recognize other visual stimuli.Balint’s Syndrome
A rare disorder of oculomotor function due to bilateral lesions of the parietal and occipital lobes.Balint’s Syndrome
Inability to move the hand towards an object by visual guidance. Dysmetria except the damage isn’t cerebellar.Optic ataxia
Paralysis and/or impairment of visual fixation, or more simply put, inability to voluntarily control one’s gaze. They seem to lack the ‘saccadic’ jump needed to acquire new visual targetsOptic apraxia
Inability to recognize more than one object at the same time. Look at place setting, can only see fork or spoon.Simultagnosia

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