Neurology - Anatomy and Physiology (1) Flashcards

1
Q

Neurons

  • Characteristics
  • Functions
  • Pathology
A
  • Characteristics
    • Permanent cells—do not divide in adulthood (and, as a general rule, have no progenitor stem cell population)
    • Signal-relaying cells with dendrites (receive input), cell bodies, and axons (send output).
    • Cell bodies and dendrites can be stained via the Nissl substance (stains RER).
      • RER is not present in the axon.
  • Functions
    • Signal-transmitting cells of the nervous system.
  • Pathology
    • If an axon is injured, it undergoes Wallerian degeneration
      • Degeneration distal to the injury and axonal retraction proximally
      • Allows for potential regeneration of axon (if in PNS).
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2
Q

Astrocytes

  • Characteristics
  • Functions
A
  • Characteristics
    • Derived from neuroectoderm
    • Astrocyte marker—GFAP
  • Functions
    • Physical support, repair, K+ metabolism, removal of excess neurotransmitter, component of blood-brain barrier, glycogen fuel reserve buffer.
    • Reactive gliosis in response to neural injury.
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3
Q

Microglia

  • Characteristics
  • Functions
  • Pathology
A
  • Characteristics
    • Mesodermal origin
    • Not readily discernible in Nissl stains
    • Have small irregular nuclei and relatively little cytoplasm
  • Functions
    • CNS phagocytes
    • Scavenger cells of the CNS
    • Respond to tissue damage by differentiating into large phagocytic cells
    • Part of the mononuclear phagocyte system.
  • Pathology
    • HIV-infected microglia fuse to form multinucleated giant cells in the CNS
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4
Q

Myelin

  • Characteristics
  • Functions
A
  • Characteristics
    • CNS—oligodendrocytes
    • PNS—Schwann cells
  • Functions
    • Increase conduction velocity of signals transmitted down axons
    • Results in saltatory conduction of action potential between nodes of Ranvier, where there are high concentrations of Na+ channels
    • Wraps and insulates axons
      • Increases space constant and increases conduction velocity.
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5
Q

Oligodendroglia

  • Characteristics
  • Functions
  • Pathology
A
  • Characteristics
    • Each oligodendrocyte can myelinate many axons (~30)
    • Predominant type of glial cell in white matter.
    • Derived from neuroectoderm
    • “Fried egg” appearance on H&E stain
  • Functions
    • Myelinates the axons of neurons in the CNS
  • Pathology
    • Injured in multiple sclerosis, progressive multifocal leukoencephalopathy (PML), and leukodystrophies.
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6
Q

Schwann cells

  • Characteristics
  • Functions
  • Pathology
A
  • Characteristics
    • Each Schwann cell myelinates only 1 PNS axon
    • Derived from neural crest.
  • Functions
    • Increase conduction velocity via saltatory conduction between nodes of Ranvier, where there are high concentrations of Na+ channels
    • Also promote axonal regeneration
  • Pathology
    • Destroyed in Guillain-Barré syndrome
    • Acoustic neuroma
      • Type of schwannoma.
      • Typically located in internal acoustic meatus (CN VIII).
      • If bilateral, strongly associated with neurofibromatosis type 2.
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7
Q

Sensory corpuscles

  • For each
    • Description
    • Location
    • Senses
  • Free nerve endings
  • Meissner corpuscles
  • Pacinian corpuscles
  • Merkel discs
A
  • Free nerve endings
    • Description:
      • C—slow, unmyelinated fibers
      • Aδ—fast, myelinated fibers
    • Location: All skin, epidermis, some viscera
    • Senses: Pain and temperature
  • Meissner corpuscles
    • Description:
      • Large, myelinated fibers
      • Adapt quickly
    • Location: Glabrous (hairless) skin
    • Senses: Dynamic, fine/light touch; position sense
  • Pacinian corpuscles
    • Description:
      • Large, myelinated fibers
      • Adapt quickly
    • Location: Deep skin layers, ligaments, and joints
    • Senses: Vibration, pressure
  • Merkel discs
    • Description:
      • Large, myelinated fibers
      • Adapt slowly
    • Location: Basal epidermal layer, hair follicles
    • Senses: Pressure, deep static touch (e.g., shapes, edges), position sense
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8
Q

Peripheral nerve

  • Endoneurium
  • Perineurium
  • Epineurium
A
  • Endoneurium
    • Invests single nerve fiber layers
    • Inflammatory infiltrate in Guillain-Barré syndrome
    • Endo = inner.
  • Perineurium
    • Permeability barrier
    • Surrounds a fascicle of nerve fibers.
    • Must be rejoined in microsurgery for limb reattachment.
    • Peri = around.
  • Epineurium
    • Dense connective tissue that surrounds entire nerve
    • Fascicles and blood vessels
    • Epi = outer.
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9
Q

Neurotransmitters

  • For each
    • Change in disease
    • Locations of synthesis
  • Norepinephrine
  • Dopamine
  • 5-HT
  • ACh
  • GABA
A
  • Norepinephrine 
    • Change in disease:
      • Increased in anxiety
      • Decreased in depression
    • Locations of synthesis: Locus ceruleus (pons)
      • Locus ceruleus— stress and panic.
  • Dopamine 
    • Change in disease:
      • Increased in Huntington disease
      • Decreased in Parkinson disease
      • Decreased in depression
    • Locations of synthesis: Ventral tegmentum and SNc (midbrain)
  • 5-HT 
    • Change in disease:
      • Increased in Parkinson disease
      • Decreased in anxiety
      • Decreased in depression
    • Locations of synthesis: Raphe nucleus (pons, medulla, midbrain)
  • ACh 
    • Change in disease:
      • Increased in Parkinson disease
      • Decreased in Alzheimer disease
      • Decreased in Huntington disease
    • Locations of synthesis: Basal nucleus of Meynert
  • GABA 
    • Change in disease:
      • Decreased in anxiety
      • Decreased in Huntington disease
    • Locations of synthesis: Nucleus accumbens
      • Nucleus accumbens and septal nucleus—reward center, pleasure, addiction, fear.
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10
Q

Blood-brain barrier

  • Functions
  • Formed by 3 structures:
  • Substances
  • A few specialized brain regions allow…
  • Other notable barriers
  • Pathology
A
  • Functions
    • Prevents circulating blood substances from reaching the CSF/CNS.
    • Helps prevent bacterial infection from spreading into the CNS
    • Also restricts drug delivery to brain
  • Formed by 3 structures:
    • Tight junctions between nonfenestrated capillary endothelial cells
    • Basement membrane
    • Astrocyte foot processes
  • Substances
    • Glucose and amino acids cross slowly by carrier-mediated transport mechanism.
    • Nonpolar/lipid-soluble substances cross rapidly via diffusion.
    • Hypothalamic inputs and outputs permeate the blood-brain barrier
  • A few specialized brain regions with fenestrated capillaries and no blood-brain barrier allow…
    • Molecules in the blood to affect brain function
      • Area postrema—vomiting after chemo
      • OVLT—osmotic sensing
    • Neurosecretory products to enter circulation
      • Neurohypophysis—ADH release
  • Other notable barriers
    • Blood-testis barrier
    • ƒƒMaternal-fetal blood barrier of placenta
  • Pathology
    • Infarction and/or neoplasm destroys endothelial cell tight junctions Ž–> vasogenic edema.
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11
Q

Hypothalamus

  • Functions
  • Inputs
  • Nuclei
    • ADH
    • Oxytocin
A
  • Functions (The hypothalamus wears TAN HATS)
    • Thirst and water balance
    • Adenohypophysis control (regulates anterior pituitary)
    • Neurohypophysis releases hormones produced in the hypothalamus
    • Hunger
    • Autonomic regulation
    • Temperature regulation
    • Sexual urges.
  • Inputs
    • Areas not protected by blood-brain barrier
    • OVLT
      • Organum vasculosum of the lamina terminalis
      • Senses change in osmolarity
    • Area postrema (responds to emetics).
  • Nuclei
    • Supraoptic nucleus makes ADH.
      • Made by hypothalamus
    • Paraventricular nucleus makes oxytocin.
      • Stored and released by posterior pituitary
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12
Q

Hypothalamus

  • Lateral area
    • Function(s)
    • Destruction –>
    • Inhibited by…
  • Ventromedial area
    • Function(s)
    • Destruction –>Ž
    • Stimulated by…
  • Anterior hypothalamus
    • Function(s)
  • Posterior hypothalamus
    • Function(s)
  • Suprachiasmatic nucleus
    • Function(s)
A
  • Lateral area
    • Hunger.
    • Destruction –>Ž anorexia, failure to thrive (infants).
    • Inhibited by leptin.
    • If you zap your lateral nucleus, you shrink laterally.
  • Ventromedial area
    • Satiety.
    • Destruction (e.g., craniopharyngioma) Ž–> hyperphagia.
    • Stimulated by leptin.
    • If you zap your ventromedial nucleus, you grow ventrally and medially.
  • Anterior hypothalamus
    • Cooling, parasympathetic.
    • Anterior nucleus = cool off (cooling, pArasympathetic).
    • A/C = Anterior Cooling.
  • Posterior hypothalamus
    • Heating, sympathetic.
    • Posterior nucleus = get fired up (heating, sympathetic).
      • If you zap your Posterior hypothalamus, you become a Poikilotherm (cold-blooded, like a snake).
  • Suprachiasmatic nucleus
    • Circadian rhythm.
    • You need sleep to be charismatic (chiasmatic).
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13
Q

Sleep physiology

  • Circadian rhythm
  • REM sleep
  • Alcohol, benzodiazepines, and barbiturates
  • Benzodiazepines
  • Norepinephrine
  • Oral desmopressin acetate (DDAVP)
A
  • Circadian rhythm
    • Sleep cycle is regulated by the circadian rhythm, which is driven by SCN of hypothalamus.
    • Circadian rhythm controls nocturnal release of ACTH, prolactin, melatonin, and norepinephrine
    • Suprachiasmatic nucleus (SCN) –>Ž norepinephrine release –>Ž pineal gland –>Ž melatonin.
    • SCN is regulated by environment (e.g., light).
    • Two stages: rapid-eye movement (REM) and non-REM.
  • REM sleep
    • Extraocular movements during REM sleep due to activity of PPRF (paramedian pontine reticular formation/conjugate gaze center).
    • REM sleep occurs every 90 minutes, and duration increases through the night.
  • Alcohol, benzodiazepines, and barbiturates
    • Associated with decreased REM sleep and delta wave sleep
  • Benzodiazepines
    • Useful for night terrors and sleepwalking
  • Norepinephrine
    • Also decreases REM sleep.
  • Oral desmopressin acetate (DDAVP)
    • Treast bedwetting (sleep enuresis)
    • Mimics ADH
    • Preferred over imipramine because of the latter’s adverse effects.
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14
Q

Sleep physiology

  • For each
    • % of total sleep time in young adults
    • Description
    • EEG waveform
  • Awake (eyes open)
  • Awake (eyes closed)
  • Non-REM sleep
    • Stage N1
    • Stage N2
    • Stage N3
  • REM sleep
A
  • Awake (eyes open)
    • %: 0%
    • Description: Alert, active mental concentration
    • EEG waveform: Beta
      • Highest frequency, lowest amplitude
  • Awake (eyes closed)
    • %: 0%
    • Description: N/A
    • EEG waveform: Alpha
  • Non-REM sleep
    • Stage N1
      • %: 5%
      • Description: Light sleep
      • EEG waveform: Theta
    • Stage N2
      • %: 45%
      • Description: Deeper sleep; when bruxism occurs
      • EEG waveform: Sleep spindles and K complexes
    • Stage N3
      • %: 25%
      • Description: Deepest non-REM sleep (slow-wave sleep)
        • When sleepwalking, night terrors, and bedwetting occur
      • EEG waveform: Delta
        • Lowest frequency, highest amplitude
  • REM sleep
    • %: 25%
    • Description: Loss of motor tone, increased brain O2 use, increased and variable pulse and blood pressure
      • When dreaming and penile/clitoral tumescence occur
      • May serve a memory processing function
    • EEG waveform: Beta
  • At night, BATS Drink Blood
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15
Q

Posterior pituitary (neurohypophysis)

A
  • Function
    • Receives hypothalamic axonal projections from supraoptic (ADH) and paraventricular (oxytocin) nuclei.
  • Oxytocin
    • Oxys = quick
    • Tocos = birth.
  • Adenohypophysis = Anterior pituitary.
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16
Q

Thalamus

  • Function
  • For each
    • Input
    • Info
    • Destination
  • VPL
  • VPM
  • LGN
  • MGN
  • VL
A
  • Function
    • Major relay for all ascending sensory information except olfaction.
  • VPL
    • Input: Spinothalamic and dorsal columns/medial lemniscus
    • Info: Pain and temperature; pressure, touch, vibration, and proprioception
    • Destination: 1° somatosensory cortex
  • VPM
    • Input: Trigeminal and gustatory pathway
    • Info: Face sensation and taste
    • Destination: 1° somatosensory cortex
    • Makeup goes on the face
  • LGN
    • Input: CN II
    • Info: Vision
    • Destination: Calcarine sulcus
    • Lateral = Light
  • MGN
    • Input: Superior olive and inferior colliculus of tectum
    • Info: Hearing
    • Destination: Auditory cortex of temporal lobe
    • Medial = Music
  • VL
    • Input: Basal ganglia, cerebellum
    • Info: Motor
    • Destination: Motor cortex
17
Q

Limbic system

  • Structures
  • Functions
A
  • Structures
    • Collection of neural structures involved in emotion, long-term memory, olfaction, behavior modulation, and autonomic nervous system function.
    • Structures include hippocampus, amygdala, fornix, mammillary bodies, and cingulate gyrus.
  • Functions (The famous 5 F’s)
    • Feeding
    • Fleeing
    • Fighting
    • Feeling
    • Sex.
18
Q

Cerebellum

  • Functions
  • Input
  • Output
  • Lateral lesions
  • Medial lesions
A
  • Functions
    • Modulates movement
    • Aids in coordination and balance.
  • Input
    • Contralateral cortex via middle cerebellar peduncle.
    • Ipsilateral proprioceptive information via inferior cerebellar peduncle from the spinal cord
    • Input nerves = climbing and mossy fibers
  • Output
    • Sends information to contralateral cortex to modulate movement.
    • ƒƒDeep nuclei (lateral Ž–> medial)
      • Dentate, Emboliform, Globose, Fastigial
      • Drink Ethanol, Go Fall”
    • Output nerves = Purkinje cells Ž–> deep nuclei of cerebellum Ž–> contralateral cortex via the superior cerebellar peduncle.
  • Lateral lesions
    • Voluntary movement of extremities
    • When injured, propensity to fall toward injured (ipsilateral) side.
  • Medial lesions
    • Lesions involving midline structures (vermal cortex, fastigial nuclei) and/or the flocculonodular lobe result in truncal ataxia, nystagmus, and head tilting.
    • These patients also may have a wide-based (cerebellar) gait and deficits in truncal coordination.
    • Generally, midline lesions result in bilateral motor deficits affecting axial and proximal limb musculature.
19
Q

Basal ganglia

  • Functions
  • Structures
    • Striatum
    • Lentiform
  • Pathways
    • Excitatory pathway
    • Inhibitory pathway
  • Dopamine binds to…
    • D1
    • D2
A
  • Functions
    • Important in voluntary movements and making postural adjustments.
    • Receives cortical input, provides negative feedback to cortex to modulate movement.
  • Structures
    • Striatum = putamen (motor) + caudate (cognitive).
    • Lentiform = putamen + globus pallidus.
  • Pathways
    • Excitatory pathway
      • Cortical inputs stimulate the striatum, stimulating the release of GABA, which disinhibits the thalamus via the GPi/SNr (increases motion).
    • Inhibitory pathway
      • Cortical inputs stimulate the striatum, which disinhibits STN via GPe, and STN stimulates GPi/SNr to inhibit the thalamus (decreases motion).
  • Dopamine binds to…
    • D1, stimulating the excitatory pathway
      • _D1-R_eceptor = D1Rect pathway.
    • D2, inhibiting the inhibitory pathway Ž–> increases motion.
      • Indirect = Inhibitory.
20
Q

Parkinson disease

  • Definition
  • Findings
A
  • Degenerative disorder of CNS associated with…
    • Lewy bodies (composed of α-synuclein— intracellular eosinophilic inclusion)
    • Loss of dopaminergic neurons (i.e., depigmentation) of the substantia nigra pars compacta.
  • Findings (Parkinson TRAPS your body)
    • Tremor (at rest— e.g., pill-rolling tremor)
    • Cogwheel Rigidity
    • Akinesia (or bradykinesia)
    • Postural instability
    • Shuffling gait.
21
Q

Huntington disease

  • Definition
  • Symptoms
A
  • Definition
    • Autosomal dominant trinucleotide repeat disorder on chromosome 4.
    • Decreased levels of GABA and ACh in the brain
    • Expansion of CAG repeats (anticipation)
      • Caudate loses ACh and GABA
  • Symptoms
    • Manifest between ages 20 and 50
    • Characterized by choreiform movements, aggression, depression, and dementia (sometimes initially mistaken for substance abuse). 
    • Neuronal death via NMDA-R binding and glutamate toxicity.
    • Atrophy of caudate nuclei can be seen on imaging.
22
Q

Movement disorders

  • For each
    • Presentation
    • Characteristic lesion
    • Notes
  • Hemiballismus
  • Chorea
  • Athetosis
  • Myoclonus [no characteristic lesion]
A
  • Hemiballismus
    • Presentation: Sudden, wild flailing of 1 arm +/- ipsilateral leg
    • Characteristic lesion: Contralateral subthalamic nucleus (e.g., lacunar stroke)
    • Notes: “Half-of-body ballistic.” Contralateral lesion.
  • Chorea
    • Presentation: Sudden, jerky, purposeless movements
    • Characteristic lesion: Basal ganglia (e.g., Huntington)
    • Notes: Chorea = dancing.
  • Athetosis
    • Presentation: Slow, writhing movements; especially seen in fingers
    • Characteristic lesion: Basal ganglia (e.g., Huntington)
    • Notes: Writhing, snake-like movement.
  • Myoclonus
    • Presentation: Sudden, brief, uncontrolled muscle contraction
    • Notes: Jerks; hiccups; common in metabolic abnormalities such as renal and liver failure.
23
Q

Movement disorders

  • For each
    • Presentation
    • Characteristic lesion
    • Notes
  • Dystonia [no characteristic lesion]
  • Essential tremor (postural tremor) [no characteristic lesion]
  • Resting tremor
  • Intention tremor [no notes]
A
  • Dystonia
    • Presentation: Sustained, involuntary muscle contractions
    • Notes: Writer’s cramp; blepharospasm (sustained eyelid twitch).
  • Essential tremor (postural tremor)
    • Presentation: Action tremor; exacerbated by holding posture/limb position
    • Notes: Genetic predisposition.
      • Patients often self-medicated with EtOH, which decreases tremor amplitude.
      • Treatment: beta-blockers, primidone.
  • Resting tremor
    • Presentation: Uncontrolled movement of distal appendages (most noticeable in hands); tremor alleviated by intentional movement
    • Characteristic lesion: Parkinson disease
    • Notes: Occurs at rest; “pill-rolling tremor” of Parkinson disease.
  • Intention tremor
    • Presentation: Slow, zigzag motion when pointing/extending toward a target
    • Characteristic lesion: Cerebellar dysfunction
24
Q

Cerebral cortex functions

A
25
Q

Homunculus

A
  • Topographical representation of motor (shown) and sensory areas in the cerebral cortex.
  • Distorted appearance is due to certain body regions that are more richly innervated and thus have increased cortical representation.
26
Q

Common brain lesions

  • Amygdala (bilateral)
  • Frontal lobe
  • Right parietal-temporal cortex
  • Left parietal-temporal cortex
  • Reticular activating system (midbrain)
A
  • Amygdala (bilateral)
    • Klüver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior)
    • Associated with HSV-1.
  • Frontal lobe
    • Disinhibition and deficits in concentration, orientation, and judgment
    • May have reemergence of primitive reflexes
  • Right parietal-temporal cortex
    • Spatial neglect syndrome (agnosia of the contralateral side of the world)
  • Left parietal-temporal cortex
    • Agraphia, acalculia, finger agnosia, and left-right disorientation
    • Gerstmann syndrome.
  • Reticular activating system (midbrain)
    • Reduced levels of arousal and wakefulness (e.g., coma)
27
Q

Common brain lesions

  • Mammillary bodies (bilateral)
  • ​Basal ganglia
  • Subthalamic nucleus
A
  • Mammillary bodies (bilateral)
    • Wernicke-Korsakoff syndrome: confusion, ophthalmoplegia, ataxia; memory loss (anterograde and retrograde amnesia), confabulation, personality changes
    • Associated with thiamine (B1) deficiency and excessive EtOH use
    • Can be precipitated by giving glucose without B1 to a B1-deficient patient.
    • Wernicke problems come in a CAN of beer: Confusion, Ataxia, Nystagmus.
  • Basal ganglia
    • May result in tremor at rest, chorea, or athetosis
    • Parkinson disease.
  • Subthalamic nucleus
    • Contralateral hemiballismus
28
Q

Common brain lesions

  • Cerebellar hemisphere
  • Cerebellar vermis
  • Hippocampus (bilateral)
  • Paramedian pontine reticular formation
  • Frontal eye fields
A
  • Cerebellar hemisphere
    • Intention tremor, limb ataxia, and loss of balance
    • Damage to the cerebellum results in ipsilateral deficits
      • Fall toward side of lesion
    • Cerebellar hemispheres are laterally located—affect lateral limbs.
  • Cerebellar vermis
    • Truncal ataxia, dysarthria
    • Vermis is centrally located—affects central body.
  • Hippocampus (bilateral)
    • Anterograde amnesia—inability to make new memories
  • Paramedian pontine reticular formation
    • Eyes look away from side of lesion
  • Frontal eye fields
    • Eyes look toward lesion
29
Q

Central pontine myelinolysis

  • Definition
  • Findings
  • Correcting too fast:
    • CPM
    • Cerebral edema/herniation
A
  • Definition
    • A variant of the osmotic demyelination syndrome.
    • Commonly iatrogenic, caused by overly rapid correction of hyponatremia
  • Findings
    • Acute paralysis, dysarthria, dysphagia, diplopia, and loss of consciousness.
    • Can cause “locked-in syndrome.”
    • Massive axonal demyelination in pontine white matter tracts [A] 2° to osmotic forces and edema.
  • Correcting serum Na+ too fast:
    • CPM: “From low to high, your pons will die”
    • Cerebral edema/herniation: “From high to low, your brain will blow”
30
Q

Aphasia

  • Aphasia
  • Dysarthria
  • Broca aphasia
  • Wernicke aphasia
A
  • Aphasia
    • Higher-order inability to speak (language deficit).
  • Dysarthria
    • Motor inability to speak (movement deficit).
  • Broca aphasia
    • Nonfluent aphasia with intact comprehension.
    • Broca area—inferior frontal gyrus of frontal lobe.
    • Broca Broken Boca (boca = mouth in Spanish).
  • Wernicke aphasia
    • Fluent aphasia with impaired comprehension and repetition.
    • Wernicke area—superior temporal gyrus of temporal lobe.
    • Wernicke is Wordy but makes no sense.
    • Wernicke = “What?”
31
Q

Aphasia

  • Global aphasia
  • Conduction aphasia
  • Transcortical motor aphasia
  • Transcortical sensory aphasia
  • Mixed transcortical aphasia
A
  • Global aphasia
    • Nonfluent aphasia with impaired comprehension.
    • Both Broca and Wernicke areas affected.
  • Conduction aphasia
    • Poor repetition but fluent speech, intact comprehension.
    • Can be caused by damage to left superior temporal lobe and/or left supramarginal gyrus.
    • Can’t repeat phrases such as, “No ifs, ands, or buts.”
  • Transcortical motor aphasia
    • Nonfluent aphasia with good comprehension and repetition.
  • Transcortical sensory aphasia
    • Poor comprehension with fluent speech and repetition.
  • Mixed transcortical aphasia
    • Nonfluent speech, poor comprehension, good repetition.
32
Q

Circle of Willis (458)

A
  • System of anastomoses between anterior and posterior blood supplies to brain.