Midterm 2 Flashcards
Brodmann’s Areas
Definition: Areas defined and numbered based on cytoarchitectural organization of neurons using the Nissl method of cell staining.
- Defined solely based on neuronal organization
- Correlate closely with diverse cortical functions
Univocal (modality-specific) association vortices
1) Primary sensory cortex
2) Primary motor cortex
3) Primary auditory cortex
4) Primary visual cortex
Heteromodal (higher-order) association cortices
1) Unimodal association cortex
2) Heteromodal association cortex
3) Prefrontal cortex
Primary Motor Cortex
Brodmann Area: 4 aka M1
Function: Works in association with premotor cortex, supplementary motor area, sensory and posterior parietal cortex and several subcortical brain regions to plan and execute movements.
- Precentral gyrus
- Contains somatotopic maps of contralateral body movements
- Target for cerebellum and motor thalamus projections
Lesion: Varied degrees of focal paralysis in the CONTRALATERAL side of the body or face.
Primary Sensory Cortex
Brodmann Area: 1, 2, 3
Function: Interlocked with primary motor cortex to send projections to the superior and inferior parietal lobules.
- Somatotopic map of contralateral body sensations
Lesion (General): Varied degrees of focal impairment in sensation on the CONTRALATERAL side.
Primary Sensory Cortex: Lesions
Acute (immediate stage): Loss of all sensory modalities on the contralateral side of body and/or face.
Chronic (later stage):
- Recovery of sensation of pain and temperature and crude touch sensation
- Thalamic level- sensation of pain and temp
- Sensory cortex- source, quality and intensity of pain
- Continued loss of fine aspects of tactile information on the contralateral body (arm and face)
- Loss of two-point discrimination
- Agraphesthesia
- Astereognosis
- Loss of vibration and light touch
- Continued loss of pro prince potion in contralateral body (arm and face)
- When leg is involved get positive Romberg sign (ataxia when eyes are closed)
Lesions to insulate and SII (maybe anterior cingulate)
Asymbolia for pain- Lack of motivation to avoid pain.
Agraphestesia
Inability to recognize a latter outlined on the skin.
Astereognosis
Inability to recognize form.
Organization and Pathways of the Somatosensory System
1) Dorsal root ganglion neurons respond to find touch adn pressure, pain and temp
2) Ventral spinothalamic tract receives input from pain and temp neurons and joins medial lemniscal tract
3) Dorsal column nuclei relay fine touch and pressure sensations.
4) Medial lemniscus contains axons that carry sensory information to the ventrolateral thalamus
5) Ventrolateral thalamus relays sensory information to the somatosensory cortex.
6) Primary somatosensory cortex receives somatosensory information.
- Homunculus
- Topographic map
- Disproportionate cortical representation of body parts
Temporal Lobe: Primary Auditory Cortex
Brodmann areas: 41, 42
- Transverse Gyri
- Represent acoustic frequencies and intensities of unhitched sounds to permit recognition and spatial localization
- Each receives input from both ears–> Unilateral damage does not cause deafness
- Surrounded by association auditory cortex
Lesion: Bilateral- auditory agnosia
Unilateral in dominant hemisphere- Pure word deafness
Unilateral in non-dominant hemisphere- Amusia (inability to produce or recognize musical sounds)
Temporal Lobe: Medial Temporal Lobe
- Cortical and subcortical structures of the limbic system
- Entorhinal cortex
- Hippocampal formation
- Amygdala
Lesion:
-Entorhinal and hippocampal formation = memory –> Anterograde memory impairment - Amygdala- Kluver-Bucy Syndrome
Kluver-Boucy Syndrome
Syndrome associated with lesions to the amygdala in which there is a marked decrease in the ability to express emotions.
Primary Visual Cortex
Lesions:
- Upper calcarine - lower field defect
- Macular sparing: Many blood vessels at the tip of the cortex for the center of vision so the center of vision is spared
- Blood from PCA and MCA
Prefrontal Cortex
- Contains areas that mediate higher mental functions
- Broca’s Area
Broca’s Area
Brodmann Area: 44, 45
- Lateral Sylvian fissure
- Pars triangularis and opercularis
- Connected to Wernicke’s area via accurate fasiculus
- Mostly in the left hemisphere because language lateralized to left (left-handed is three way split between left, right and both) - Language distinct from speech- speech supported by the entire motor system for vocalization
Arcuate fasiculus
Structure that connects Wernicke’s and Broca’s areas
Association Sensory Cortex
- Superior and inferior parietal lobules
- Connects Wernicke’s and Broca’s areas
Lesion: - Dominant hemisphere
- Inferior parietal lobule
- Angular gyrus: Alexia and agraphia (inability to read written language and inability to write language)
- Supramarginal gyrus: Conduction aphasia
- Superior parietal lobule- Optic ataxia in contralateral hand
- Can’t use the visual system to guide motor movements so reaching for anything is like reaching into the dark - Non-dominant hemisphere
- Inferior parietal lobule- Anosagnosia (unaware of their condition)
- Left visual field neglect (can’t follow previously known and automated route, not hit obstacles on left side, can’t learn new route) - Superior parietal lobule- Optic ataxia
- Inferior parietal lobule- Anosagnosia (unaware of their condition)
Object Agnosia
- Bilateral inferolateral parts of occipital lobes
- Patient fails to name or indicate the use of a seen object
- Vision is intact because patient can see an object but can’t tell what it is
- If object is touched or smelled or makes a sound then it can be recognized
Achromatopsia
Failure to recognize color.
- Inferior occipital cortices
- Sparing calcarine cortex
- Contralateral
Prosopagnosia
Inability to recognize faces but able to see the face.
- Bilateral occipitotemporal
Anton’s Syndrome
Denial of blindness
- Bilateral occipital cortices from calcarine and extending superiorly to parietal cortex.
Anatomical and Functional Asymmetry
- Slope of lateral (sylvian) fissure differs
- Wernicke’s area mostly left hemisphere
- More auditory cortex in the left
- Left more verbal and right is more non-verbal
- Left temporal lobectomy: Low verbal recall
- Right temporal lobectomy: Low non-verbal recall (performance IQ too, but may be unrelated)
Commissurotomy
Split brain
- Put object in left hand, patient cannot name object but if you put the same object in the right hand patient can name it
The Wada Test
Function: Determines which side language is lateralized on before surgery
- Sodium amobarbital injected into carotid artery where it anesthetizes the hemisphere on the side of injection
- On left side patient shouldn’t be able to speak if speech is lateralized there
Damage to right parietal cortex
Anosognosia
- Denial of illness or failure to recognize
- Apathy/placidity
- Paralyzed on left side of body but say they could move it, or reason that they don’t need that side so it’s okay
- After a while they will come to accept that they’ve had a stroke but still not full acceptance like a normal patient - Left-sided damage leads to aphasia and patients are cognizant of their deficit and often feel depressed
Clinical Case: What functional sensory and motor systems are affected in this patient?
1) Upper Motor Lesion: Inability to grasp, dragging left leg and Babinski’s sign
- Corticospinal tract: Arm and leg involved, above C4
- Facial nerve: Above level of facial nuclei because of lower face paralysis
2) Somatosensory cortex: Intact primary modalities (pain and temperature) but loss of cortical modalities (proprioception, graphesthesia, two-point discrimination, localization of light touch) on left side –> Only occurs when the thalamus is spared
(In other words: intact elementary sensation and impaired discriminative sensation suggest a lesion of right hemisphere rostrum to the right thalamus)
Clinical Case: At what level of the CNS are they affected?
Cortex
(Evidence: Somatosensory cortex damage- primary modalities in tact like pain and temperature/touch, but cortical modalities like proprioception and graphesthesia and two-point discrimination aren’t in good shape)
(Evidence: Right-sided lesion between frontal eye fields and midbrain would affect corticospinal tract which explains left-sided weakness, and cause left gaze paresis because damage to these circuits causes contralateral eye deviations and the eye deviates to the left)
(Evidence: Supranuclear disorder of gaze- oculovestibular functions intact (doll’s head) but can’t move voluntary –> Lesion must be above the level of Rochelle, oculomoter and abducens nuclei and nerves and the. Medial longitudinal fasiculus is intact)
Clinical Case: Why is the patient’s gaze direct to the right?
Lesions in the right side of the brain cause left gaze palsy.
Clinical Case: Why does the patient have a left gaze palsy?
The patient cannot move their eyes to the left because of frontal eye field lesions.
- Stimulation causes ipsilateral deviation and destructive lesions cause the eyes to deviate contra-laterally
- Lesion above the lower midbrain of pathways from the right frontal eye fields will prevent the patient from looking to the contralateral side - Frontopontine tract from motor cortex to PPRF on contralateral side, right near motor facial representation
- Lesions cause eyes to deviate to the side of lesion
- Lesion above lower midbrain of patient in pathways from FEF will prevent patient from being able to make left gaze
Clinical Case: How would you test this patient’s vestibule-ocular movements?
You would use doll’s head movements- Changing vestibular system causes the eyes to move to maintain fixation as the head moves.
Clinical Case: Discuss the patient’s visual sensory deficit and provide the appropriate neurological/opthamological name for it.
Name: A left homonymous hemianopsia
- Follows right-sided lesions of the retrochiasmal afferent visual system which includes the optic tract, lateral geniculate nucleus, optic radiations and occipital cortex.
- Some of these regions past the chiasm cause foveal sparing, so it must be optic radiations
- Optic radiations are just near the motor and sensory cortex and frontal eye fields, so extend the lesion to these areas and anatomical diagnosis is complete
Clinical Case: Why is the abrupt onset of symptoms significant for this patient?
Symptoms that quickly appear usually indicate a vascular incident (stroke), or electrical incident. The patient likely does not have a tumor since those grow gradually and progressively affect behavior and generate deficits.
- Vascular has negative symptoms while electrical has positive --> This case is all negative symptoms so it's vascular and from occlusion because no headache - Middle cerebral artery stroke because that supplies most of motor and sensory cortices as well as frontal eyes fields which is all the stuff affected in this case - Supplies optic radiations as well- responsible for gaze problems - Patient's diabetes mellitus and hypertension increase risk for antherosclerotic disease, making ischemic stroke even more likely
Clinical Case: Cause of stroke
Emobolus from left atrium to right middle cerebral artery.
Posterior Cerebral Artery supplies….
Visual cortex, upper brain stem and inferior temporal lobe
Anterior cerebral artery supplies….
Frontal and medial cerebrum - strokes cause lower extremity sensory and motor loss.
Middle cerebral artery supplies….
Lateral aspects of the cerebrum including most of the sensory-motor cortices and frontal eye fields. Also supplies underlying white matter like the optic radiations
- Stroke in this area creates pattern of symptoms described in this case
Five elements of a neurological exam
1) Cranial nerves
2) Motor system
3) Sensory system
4) Coordination/balance/gait
5) Mental status
Which cranial nerves provide taste?
Facial, gossopharyngeal and vagus
7, 9 and 10
Clinical Tests: Cranial Nerve I (Olfactory)
Testing: Smell
- Damage can lead to traumatic anosmia
- A special kit has numerous packets that store various smells. The examiner scratches one packet at a time and asks the patient to identify the smell.
- This is done by closing one nostril and testing the other.
