Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FA13 Neurology > Neuro-01-Emrbyo_Physio_Anat > Flashcards

Neuro-01-Emrbyo_Physio_Anat Flashcards

1
Q

Development of neural tube and neural crest

A

• Occurs from day 18 to day 21

  1. The Notochord induces the overlying ectoderm to differentiate into neuroectoderm and form the neural plate
  2. the neural plate folds inward and gives rise to the neural tube, and the cells from the fold will become the neural crest
  3. The Notochord weill become the nucleus pulposus of the intervertebral discs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Alar and Basal plate

A
  • The intermediate zone of the early neural tube has an alar plate and basal plate
  • Alar plate (dorsal): sensory
  • Basal plate (ventral): motor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Vesicles of developping brain

A
  • 3 vesicle stage:
    • Prosencephalon (Forebrain)
    • Mesencephalon (Midbrain)
    • Rhombencephalon (hindbrain)
  • 5 vesicle stage:
    • Telencephalon -> cerebral hemispheres; lateral ventricles
    • Diencephalon -> thalamus; third ventricle
    • Mesencephalon -> midbrain; cerebral aqueduct
    • Metencephalon -> pons, cerebellum; upper part of fourth ventricle
    • Myelencephalon -> Medulla; lower part of fourth ventircle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Neural tube defects

A
  • Due to a failure of fusion of the Neuropores (happens around the fourth week)
  • This leads to a persistent connection between the amniotic cavity and the spinal canal
  • They are associated with low folic acid intake before conception
  • Findings:
    • Elevated alpha-fetoprotein (AFP) in amniotic fluid and maternal serum
    • Elevated acetylcholinesterase (AChE) in amniotic fluid is a helpful confirmatory test (it lesks out from the fetal CSF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Spina bifida occulta

A
  • Failure of bony spinal canal to close, but there is no structural herniation
  • Usually seen at lower vertebral levels
  • Dura is intact
  • Associated with tuft of hair or skin dimple at level of bony defect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Meningocele

A

Meninges (but not the spinal cord) herniate through spinal canal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Meningomycele

A

Both the meninges and the psinal cord herniate through the spinal canal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Anencephaly

A
  • Malformation of anterior neural tube resulting in no forebrain, open calvarium (“frog-like apperance”)
  • Associated with maternal diabetes (type I)
  • Maternal folate supplementation decreases risk
  • Findings:
    • Increased AFP
    • Polyhydramnios, because there is no swallowing center in brin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Holoprosencephaly

A
  • Failure of hemispheres to separate, usually during weeks 5-6
  • Complex multifactorial etiology; may be related to mutations in sonic hedgehog sinaling pathway
  • Moderate form has cleft lifp/palate
  • Most severe form results in cyclopia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Chiari II (Arnold-Chiari) malformation

A
  • Significant herniation of cerebellar tonsils and vermis through the foramen magnum
  • Leads to aqueductal stenosis and hydrocephalus
  • Often presents with thoraco-lumbar myelomeningocele and paralysis below the defect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Dandy-Walker malformation

A
  • Agenesis of cerebellar vermis
  • Cystic enlargement of 4th ventricle (fills the enlarged posterior fossa)
  • Associated with hydrocephalus and spina bifida
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Derivatives of Nueroectoderm

A
  • CNS neurons
  • Ependymal cells (line ventricles; make CSF)
  • Oligodendroglia
  • Astrocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Derivatives of Neural crest

A
  • PNS neurons

* Schwann cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Derivatives of Mesoderm

A

Microglia (e.g., Macrophages) {Microglia like Macrophages originate from Mesoderm}

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Properties of Neurons

A
  • Signal-ptransmitting cells of the nervous system
  • Permanent cells–do not divide in adulthood; as a general rule, have no progenitor stem cell population
  • Dendrites receive input, and axons send output
  • Cell bodies and dendrites can be stained via Nissl substance (stains RER), since RER is not present in the axon
  • Axon injury leads to Wallerian degeneration: degeneration distal to injury, and axonal retraction proximally; allows for potential regeneration of axon (if in PNS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Properties of Astrocytes

A
  • Physical support and repair in CNS
  • K+ metabolism
  • Removal of excess neurotransmitter
  • Maintain the blood-brain barier
  • Reactive gliosis in response to injury
  • GFAP is marker for astrocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Properties o Microglia

A
  • CNS phagocytes of mesodermal origin
  • Not readily discernible in nNissl stains
  • Hame small, irregular nuclei and relatively little cytoplasm
  • Scavenger cells of the CNS
  • Respond to tissue damage by differentiating into large phagocytic cells
  • HIV -infected microglia fuse to form multinuclated giant cells in the CNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Properties of Myelin

A
  • Wrap and insulate axons, leading to increased space constant and increased conduction velocity
  • Increase conduction velocity of signals transmitted down axons
  • Lead to saltatory conduction of action potentials between nodes of ranvier (where there are high concentrations of Na+ channels)
  • Oligodendrocytes (CNS) and Schwann cells (PNS) are the myellinating cells of nervous system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Properties of oligodendroglia

A
  • Each oligodendrocyte myelinates multiple CNS axons (up to 50 each)
  • In Nissl stain, they appear as small nuclei with dark chromatin and little cytoplasm
  • Predominant type of glial cell in white matter
  • Look like fried eggs on H&E stains
  • Oligondendrocytes are destroyed in multiple sclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Properties of Schwann cells

A
  • Each Schwann cell myelinates only one PNS axon
  • Also promote axonal regeneration
  • Derived from neural crest
  • Schwann cells are destroyed in Guillain-Barre syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Acoustic neuroma

A

Type of schwannoma typically located in internal acoustic meatus (CN VIII)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Free nerve endings

A
  • Can be C fibers (slow, unmyelinated)
  • Or can be A-delta fibers (fast, myelinated)
  • Located on all skin, epidermis, and some viscera
  • Sense pain and temperature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Meissner’s corpuscles

A
  • Large, myelinated fibers
  • adapt quickly
  • Located on glabrous (hairless) skin
  • Sense dynamic, fine/light touch, position sense
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pacinian corpuscles

A
  • Large, myelinated fibers
  • Located in deep skin layers, ligaments, and joints
  • Sense vibration, pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Merkel’s discs

A
  • Large, myelinated fibers
  • adapt slowly
  • Located on hair follicles
  • Sense pressure, deep sstatic touch (e.g., shapes, edges), position sense
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Structure of peripheral nerves

A
  • Endoneurium invests single nerve fiber layres
    • There is inflammatory infiltrate in Guillain-Barre
  • Perineurium (Permeability barrier) surrounds a fascicle of nerve fibers
    • Must be rejoined in microsurgery for limb reattachment
    • Epineurium is a dense connective tissue that sourrounds the entire nerve, including fasicles and blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Synthesis and change in disease of Norepinephrine (NE)

A
  • Synthesized in Locus ceruleus (Pons)
  • increased in anxiety
  • Decreased in depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Synthesis and change in disease of Dopamine

A
  • Synthesized in ventral tegmentum and SNc (midbrain)
  • Increased in schizophrenia
  • Decreased in depression
  • Decreased in Parkinson’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Synthesis and change in disease of Serotonin (5-HT)

A
  • Synthesized in Raphe nucleus (pons)
  • Decreased in anxiety
  • Decreased in depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Synthesis and change in disease of Acetylcholine (ACh)

A
  • Synthesized in Basal nucleus of Meynert
  • Decreased in Alzheimer’s
  • Decreased in Huntington’s
  • Increased in REM sleep
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Synthesis and change in disease of GABA

A
  • Synthesized in Nucleus accumbens
  • Decreased in anxiety
  • Decreased in Huntington’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Behavior associations of Locus ceruleus

A

Stress and panic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Behavior associations of Nucleus accumbens and spetal nucleus

A

Reward center, pleasure, addiction, fear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Blood-brain barrier (BBB)

A
  • Prevents circulating blood substances or bacteria from reaching the CSF/CNS
  • Restricts drug delivery to the brain
  • Formed by 3 structures:
    • Tight junctions between nonfenestrated capillary endothelial cells
    • Basement membrane
    • Astrocyte foot processes
  • Glucose and amino acids cross slowly by carrier-mediated transport mechanism
  • Nonpolar/lipid-soluble substances cross rapidly via diffusion
  • Infarction and/or neoplasm destroys endothelial cell tight junctions, leading to vasogenic edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Regions of brain with fenestrated capillaries and no BBB

A
  • Allow molecules in the blood to affect brain function (e.g., area postrema - vomiting after chemo; OVLT - osmotic sensing)
  • Allow neurosecretory products to enter circulation (e.g., Neurohypophysis - ADH release)
  • Hypothalamic inputs and outputs permeate the BBB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Other notable blood barriers

A
  • Blood-testis barrier

* Maternal-fetal blood barrier of placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Function of the Hypothalamus

A
  • Inputs (these areas are not protected by the BBB):
    • OVLT: sense change in osmolarity
    • Area postrema: responds to emetics
  • {TAN HATS}
  • Thirst and water balance
  • Adenohypophysis (anterior pituitary) control via hormones
  • Neurohypophysis (posterior pituitary) releases hormones produced in the hypothalamus
  • Hunger
  • Autonomic regulation
  • Temperature regulation
  • Sexual urges
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Lateral area of the hypothalamus

A
  • Positively controls hunger {If you zap your lateral nucleus, you shring laterally}
  • Inhibited by leptin
  • Destruction leads to anorexia, failure to thrive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Ventromedial area

A
  • Positively controls satiety {If you zap your ventromedial nucleus, you grow ventrally and medially}
  • Stimulated by leptin
  • Destruction (e.g., craniopharyngioma) leads to hyperphagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Anterior hypothalamus

A
  • Positively controls cooling {Anterior nucleus = Cooling, pArasympthatic; A/C}
  • Parasympathetic control
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Posterior hypothalamus

A
  • Positively controls Heating {If you zap your Posterior hypothalamus, you become a poikilotherm (cold-blooded, like a snake)
  • Sympathetic control
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Suprachiasmatic nucleus

A

Controls circaidan rhythm {You need sleep to be charismatic (chiasmatic)}

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Posterior pituitary (neurohypophysis)

A
  • ADH and oxytocin are madeby the hypothalamus but are stored and released by the posterior pituitary
  • Receives hypothalamic axonal projections from supraoptic (ADH) and paraventricular (oxytocin) nuclei
  • Oxys = quick; tocos = birth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Function of the thalamus

A
  • Major relay for all ascending sensory information (except olfaction)
  • Nuclei:
    • Ventral posterolateral (VPL) nucleus
    • Ventral posteromedial (VPM) nucleus
    • Lateral geniculate nucleus (LGN)
    • Medial geniculate nucleus (MGN)
    • Ventral lateral (VL) nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Ventral posterolateral (VPL) nucleus of the thalamus

A
  • Input: spinothalamic and dorsal column/medial lemniscus
  • Information: Pain and temperature, pressure, touch, vibration, and proprioception
  • Destination: Primary somatosensory cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Ventral posteromedial (VPM) nucleus of the thalamus

A
  • Input: trigeminal and gustatory pathway
  • Information: face sensation and taste
  • Destination: primary somatosensory cortex
  • {Makeup goes on the face (VPM)}
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Lateral geniculate nucleus (LGN) of the thalamus

A
  • Input: CN II
  • Information: vision
  • Destination: Calcarine sulcus
  • {Lateral = Light}
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Medial geniculate nucleus (MGN) of the thalamus

A
  • Input: Superior olive and inferior colliculus of tectum
  • Information: Hearing
  • Destination: Auditory cortex of temporal lobe
  • {Medial = Music}
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Ventral lateral (VL) nucleus of the thalamus

A
  • Input: Basal ganglia
  • Information: Motor
  • Destination: Motor cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Limbic system

A
  • Collection of neural structures involved in emotion, long-term memory, olfaction, behavior modulation, and autonomic nervous system function
  • Structures:
    • Hippocampus
    • Amygdala
    • Fornix
    • Mammillary bodies
    • Cingulate gyrus
  • {5 F’s: Feeding, Fleeing, Fighting, Feeling, Sex}
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Cerebellum

A
  • Modulates movement; aids in coordination and balance
  • Input: {Ipsilateral to body, while brain is contralateral}
    • Contralatera 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
    • Output nerves: pirkinje fibers send information to depe nuclei of cerebellum, which in turn send information to the contralateral cortex via the superior cerebellar peduncle
    • Deep nuclei (from lateral to medial): Dentate, Emboliform, Globose, Fastigial {Don’t Eat Greasy Foods}
  • Lateral cerebellum: voluntary movement of extremities
    • When injured, there is a propensity to fall toward ipsilateral side
  • Medial cerebellum: Balance, truncal coordination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Function of Basal Ganglia

A
  • Important in voluntary movements and maing postural adjustements
  • Receives cortical input, provides negative feedback to cortex to modulate movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Components of striatum

A
  • Putamen (motor)
  • Caudate (cognitive)
  • Anatomically and functionally related
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Components of lentiform

A
  • Putamen
  • Globus pallidus
  • Neighboring nuclei with different functions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Components of substantia nigra

A
  • Substantia nigra pars compacta (SN-C): nigrostriatal dopaminergic neurons
  • Substantia nigra pars reticulata (SN-R) similar to globus pallidus interna
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Basal ganglia direct (stimulatory) pathway

A
  1. The cortext stimulates the striatum via Glu
  2. The striatum inhibits the GPi/SN-R via GABA
  3. The GPi/SN-R usually inhibits the thalamus via GABA
  4. The Thalamus stimulates the Cortex via Glu
    • End result: The thalamus is disinhibited, resulting in stimulation of movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Basal ganglia indirect (inhibitory) pathway

A
  1. The cortext stimulates the striatum via Glu
  2. The striatum inhibits the GPe via GABA
  3. The GPe usually inhibits the STN via GABA
  4. The STN usually stimulates the GPi/SNR via Glu
  5. The GPi/SNR inhibits the thalamus via GABA
  6. The thalamus usually stimulates the cortex via Glu
    • End result: the STN is disinhibited, which inhibits the thalamus, resulting in inhibition of movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Modulation of direct and indirect pathways by the SNc via Dopamine

A
  • Dopamine binds to D1 receptors in striatum, stimulating the direct pathway; this leads to stimulation of motion
  • Dopamine binds to D2 receptors in striatum, inhibiting the indirect; this leads to stimulation of motion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Parkinson’s disease

A
  • Degenerative disorder of CNS associated with Lewy body inclusions (composed of alpha-synuclein)
  • Leads to loss of dopaminergic neurons (depigmentation) of substantia nigra pars compacta
  • Findings: {your body becomes a TRAP}
    • Tremor at rest (e.g., pill-rolling remor)
    • cogwheel Rigidity
    • Akinesia or bradykinesia
    • Postural instability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Huntington’s disease

A
  • Autosomal-dominant trinucleotide repeat (CAG); anticipation
  • Caudate loses ACh and GABA
  • Leads to loss of striatal projections to Gpe; this leads to disruption of indirect pathway, leading to incrased movement
    • Neuronal death via NMDA-R binding and glutamate toxicity
  • Atrophy of striatal nuclei can be seen on imaging
  • Presentation:
    • Chorea
    • aggression
    • depression
    • dementia
    • Can sometimes be mistaken for substance abuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Hemiballismus

A
  • Sudden, wild flailing of 1 arm and maybe the ipsilateral leg
  • Characteristic Lesion: Contralateral subthalamic nucleus (e.g., lacunar stroke)
  • {Half of body ballistic}
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Chorea

A
  • Sudden, jerky, purposeless movements
  • Characteristic lesion: Basal ganglia (e.g., Huntington’s)
  • (Chorea = dancing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Athetosis

A
  • Slow, writhing, snake-like movements; especially seen in fingers
  • Characteristic lesion: Basal ganglia (e.g., Huntington’s)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Myoclonus

A
  • Sudden, brief, uncontrolled muscle contraction (e.g., jerks, hiccups)
  • Common in metabolic abnormalities such as renal and liver failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Dystonia

A
  • Sustained, involuntary muscle contractions (e.g., Writer’s cramp, blepharospasm)
  • Sporadic torticollis (neck) is the most common type of dystonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Essential tremor (postural tremor)

A
  • Action tremor; exarcerbated by holding posture/limb position
  • Genetic predisposition
  • Patients often self-medicated with EtOH, which reduced tremor amplitude
  • Treatment: beta-blocers, primidone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Resting tremor

A
  • Unctonrolled movement of distal appendages (most noticeable in hands–“pill-rolling tremor”)
  • Tremor alleviated by intentional movement
  • Characteristic lesion: Parkinson’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Intention tremor

A
  • Slow, zigzag motion when pointing/extending toward a target
  • Characteristic lesion: cerebellar dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Important areas in Frontal lobe

A
  • Principal motor area
  • Premotor area (part of extrapyramidal circuit)
  • Frontal eye fields
  • Motor speech (Broca’s area; dominant hemisphere)
  • Frontal association areas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Important areas in Parietal lobe

A
  • Principal sensory areas

* Arcuate fasciculus (damage leads to conduction aphasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Important areas of the occippital lobe

A

Principal visual cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Important parts of the Temporal lobe

A
  • Primary auditory cortex

* Associate auditory cortex (Wernicke’s area; dominant hemisphere)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Homunculus

A
  • Topographical representation of sensory and motor areas in the cerebral cortex
  • Can be used to localize lesion leading to specific defects (e.g., lower extremity deficit may indicate involvement of the ACA)
  • Arrangement:
    • Lower extremities medially, upper extremities more laterally
    • Face is more lateral than upper extremity, but forehead is more medial and lips are more lateral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Consequence of lesion of Amygdala (bilateral)

A
  • Kluver-Bucy syndrome: hyperorality, hypersexuality, disinhibited behavior
  • Associated with HSV-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Consequence of lesion of Frontal lobe

A
  • Disinhibition and deficits in concentration, orientation, and judgement
  • May have reemergence of primitive reflexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Consequence of lesion of right parietal lobe

A
  • Spatial neglect syndrome: agnosia of the contralateral side of the world
  • Normally, right hemisphere is directed to both sides, whicle the left hemisphere is mainly concerned with the right (contralateral) side
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Consequence of lesion of Reticular activating system (midbrain)

A

Reduced levels of arousal and wakefulness (e.g., coma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Consequence of lesion of Mammillary bodies (bilateral)

A
  • Wernicke-Korsakoff syndrome: confusion, opthalmoplegia, 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Consequence of lesion of Basal ganglia

A
  • May result in tremor at rest, chorea, or athetosis

* Associated with Parkinson’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Consequence of lesion of Cerebellar hemisphere

A
  • 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}
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Consequence of lesion of Cerebellar vermis

A
  • Truncal ataxia, dysarthria

* {Vermis is centrally located - affects central body}

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Consequence of lesion of Subthalamic nucleus

A

Contralateral hemiballismus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Consequence of lesion of Hippocampus

A

Anterograde amnesia: inability to make new memories

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Consequence of lesion of Paramedian pontine reticular formation (PRRF)

A
  • Eyes look away from side of lesion

* Usually the PPRF “pulls” eyes to its side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Consequence of lesion of Frontal eye fields

A
  • Eyes look toward lesion

* Usually the FEF “push” eyes away from its side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Central pontine myelinolysis

A
  • Massive axonal demyelinatio in pontine white matter tracts
  • Commonly caused by overly rapid correction of Na+ levels
  • Leads to acute paralysis, dysarthria, diplopia, and loss of consciousness
  • Can caouse locked-in syndrome
  • T2-weighted MRI with FLAIR shows abnormal increased signal incentral pons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Location of Broca’s area

A

Inferior frontal gyrus of frontal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Location of Wernicke’s area

A

Superior temporal gyrus of temporal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Aphasia vs. dysarthria

A
  • Aphasia: higher-order inability to speak (language deficit)
  • Dysarthria: Motor inability to speak (movement deficit)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Broca’s aphasia

A
  • Nonfluent aphasia with intact comprehension

* {Broca’s Broken Boca}

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Wernicke’s aphasia

A
  • Fluent aphasia with impaired comphrehension

* {Wernicke’s is wordy but makes no sense; Wernicke’s = what}

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Global aphasia

A
  • Nonfluent aphasia with impoaire dcomprehension

* Booth Broca’s and Wernicke’s areas affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Conduction aphasia

A
  • Poor repetition but fluent speech and intact comprehension
  • Can’t repeat phrases such as “No ifs, ands, or buts”
  • Can be caused by damage to arcuate fasciculus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Arteries supplying the cortex

A
  • Anterior cerebral artery supplies anteromedial surface
  • Middle cerebral artery supplies lateral surface
  • Posterior cerebral artoery supplies posterior and inferior surfaces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Watershed zones

A
  • Between anterior cerebral and middle cerebral, or between posterior cerebral and meiddle cerebral arteries
  • Damaged in severe hypertesion
  • Would lead to upper leg or upper arm wakness, defects in higher-order visual processing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Regulation of cerebral perfusion

A
  • Brain perfusion relies on tight autoregulation that is mainly driven by PCO2 (PO2 also modulates perfusion in severe hypoxia)
  • Therapeutic hyperventilation (decreases PCO2) helps decrease intracranial presure in cases of acute cerebral edema (stroke, trauma) via decreasing cerebral perfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Effect of stroke in MCA (middle cerebral artery)

A
  • Motor cortex (upper limb and face): contralateral paralysis of upper limb and face
  • Sensory cortex (upper limb and face): contralateral loss of sensation of upper limb and face
  • Temporal (Wernicke’s area) or frontal (Broca’s area) lobe: Aphasia if in dominant hemisphere (usually left); hemineglect if lesion affects nondominant side (usually right)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Effect of stroke in ACA (anterior cerebral artery)

A
  • Motor cortex (lower limb): Contralateral paralysys of lower limb
  • Sensory cortex (lower limb): Contralateral loss of sensation of lower limb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Effect of stroke in Lateral striate artery (branch of MCA)

A
  • Striatum, internal capsule: contralateral hemiparesis (weakness) or hemiplegia (paralysis)
  • Common location of lacunar infarcts; secondary to unmanaged hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Effect of stroke in ASA (anterior spinal artery)

A
  • Lateral corticospinal tract: contralateral hemiparesis (lower limbs)
  • Medial lemniscus: decreased contralateral proprioception
  • Caudal medulla (hypoglossal nerve): Ipsilateral hypoglossal dysfunction (tongue deviates ipsilaterally)
  • Stroke commonly bilateral
  • Medial medullary syndrome: causd by infarct of paramedian branches of ASA and vertebral arteries: leads to the symptoms described above
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Effect of stroke in PICA (Posterior inferior cerebellar artery)

A
  • Lateral medulla (vestibular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguus, sympathetic fibers, inferior cerebellar peduncle): Vomiting, vertigo, nystagmus, decreased pain and temperature sensation to limbs and face, dysphagia, hoarseness, decreased gag reflex, ipsilateral horner’s syndrome, ataxia, dysmetria
  • Nucleus ambiguus effects are specific to PICA lesions {Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia)}
  • Lateral medullary (Wallenberg’s syndrome) leads to the symptoms described above
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Effect of stroke in AICA (anterior inferior cerebellar artery)

A
  • Lateral pons (cranial nerve nuclei, vestibular nuclei, facial nucleus, spinal trigeminal nucleus, cochlear nuclei, sympathetic fibers): Vomiting, vertigo, nystagmus, paralysis of face, decreased lacrimation, salivation, decreased taste from anterior 2/3 of tongue, decreased corneal reflex, decreased pain and temperature sensation on face, ipsilateral hearing loss, ipsilateral horner’s syndrome)
  • Facial nucleus effects are specific to AICA lesions {Facial droop means AICA’s pooped}
  • Lateral pontine syndrome leads to symptoms described above
  • Middle and inferior cerebellar peduncles: Ataxia, dysmetria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Effect of stroke on PCA (posterior cerebral artery)

A

• Occipital cortex, visual cortex: contralateral hemianopia with macular sparing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Effect of lesion on Anterior communicating artery

A
  • Common site of sacular (berry) anneurism, leading to impingement on cranial nerves: visual field defects
  • Lesions are typically aneurysms, not strokes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Effect of lesion on Posterior communicating artery

A
  • Common site of sacular (berry) aneurysm: CN III palsy - eye is “down and out” with ptosis and pupil dilatation
  • Lesions are typically aneurysms, not strokes
106
Q

Definition of aneurysm

A

An abnormal dilatation of artery due to weakening of vessel wall

107
Q

Berry aneurysm

A
  • Occurs at the bifurcations in the circle of Willis
  • Most common site is the bifurcation of the anterior communicating artery
  • Rupture (most common complication) leads to subarachnoid hemorrhage (“worst headache of life”) or hemorrhagic stroke
  • Can cause bitemporala hemianopia via compression of the optic chiasm
  • Associated with:
    • ADPKD
    • Ehlers-Danlos syndrome
    • Marfan’s syndrome
    • Advanced age
    • Hypertension
    • Smoking
    • Race (higher risk in blacks)
108
Q

Charcot-Bouchard microaneurysm

A
  • Associated with chronic hypertension

* Affects small vessels (e.g., in basal ganglia, thalamus)

109
Q

Epidural hematoma

A
  • Usually due to a ruputure of the middle meningeal artery (Branch of maxillary artery)
  • Often secondary to fracture of temporal bone
  • There is a lucid interval
  • Rapid expansion under systemic arterial pressure leads to transtentorial herniation and CN III palsy
  • CT shows biconvex (lentiform), hyperdense blood collection that does not cross suture lines
  • Can cross falx, tentorium
110
Q

Subdural hematoma

A
  • Usually due to a ruputure of bridging veins, leading to slow venous bleeding (less pressure leads to hematoma developing over time)
  • Seen in elderly individuals, alcoholics, blunt trauma, shaken baby
  • Predisposing factors: Brain atrophy, shaking, whiplash
  • Cresent-shaped hemorrhage that crosses suture line
  • There can be midline shift
  • Cannot cross falx, tentorium
111
Q

Subarachnoid hemorrhage

A
  • Rupture of an aneurysm, such as berry (sacular) aneurysm, or an AVM (arteriovenous malformation)
  • Rapid time course
  • Patients’ complain of “worst headache of my life”
  • Bloody or yellow (xanthochromic) spinal tap
  • Risk of vasopasm 2-3 days afterward due to blood breakdown (not visible on CT, treat with nimodipine) and rebleed (visible on CT)
112
Q

Intraparenchymal (hypertensive) hemorrhage

A
  • Most commonly caused by systemic hypertension
    • Also seen with amyloid angiopathy, vasculitis, and neoplasm
  • Typically occurs in basal ganglia and internal capsule (Charcot-Bouchard eneurysm of lenticulostriate vessels), but can be lobar
113
Q

Progression of irreversible neuronal injury after ischemia/stroke

A

• Irreversible damage begins after 5 minutes of hypoxia

  1. red neurons (12-48 hours)
  2. necrosis and neutrophils (24-72 hours)
  3. macrophages (3-5 days)
  4. reactive gliosis and vascular proliferation (1-2 weeks)
  5. glial scar (>2 weeks)
114
Q

Most vulnerable areas to ischemia/stroke

A
  • Hippocampus
  • Neocortex
  • Cerebellum
  • Watershed areas
115
Q

Stroke imaging

A
  • Ischemic stroke appears bright on diffusion-weighted MRI in 3-30 minutes and remains bright for 10 days
  • Ischemic stroke appears dark on noncontrast CT in ~ 24 hours
  • Hemorrhage appears bright on noncontrast CT (tPA contraindicated)
116
Q

Role of atherosclerosis in stroke

A
  • Thrombi lead to schemic stroke with subsequent necrosis

* Form cystic cavity with reactive gliosis

117
Q

Hemorrhagic stroke

A
  • Intracerebral bleeding, often due to hypertension, anticoagulation, and cancer (abnormal vessels can bleed)
  • may be secondary to ischemic stroke followed by reperfussion (there is an increase in vessel fragility)
118
Q

Ischemic stroke

A
  • Atherosclerotic emboli block large vessels
  • Etiologies include atrial fibrillation, carotid dissection, patent foramen ovale, endocarditis
  • Lacunar strokes block small vessels, may be secondary to hypertension
  • Treatment: tPA within 4.5 hours (so long as patient presents within 3 hhours onset and there is no major risk of hemorrhage)
119
Q

Transient ischemic attack

A
  • Brief, reversible episode of focal neurologic dysfunction, typically lasting < 24 hours without acute infarction (negative MRI)
  • Deficits are due to focal ischemia
  • Most resolve in within an hour
120
Q

Dural venous sinuses

A
  • Large venous channels that run through the dura
  • Drain blood from cerebral veins and receive CSF from arachnoid granulations
  • Empty into internal jugular vein
  • Important ones: Superior sagittal sinus, Inferior sagittal sinus, Straight sinus, Great cerebral vein of galen, confluence of the sinuses, occipital sinus, transverse sinus, sigmoid sinus (IJV), superior petrosal sinus, inferior petrosal sinus, cavernous sinus, sphenoparietal sinus, superior ophthalmic vein
121
Q

CSF circulation in brain

A
  • CSF is made by ependymal cells of choroid plexus
  • CSF reasbsorbed by arachnoid granulations into dural venous sinuses
  • From lateral ventricle to third ventricle via foramina of Monro
  • From third ventricle to fourth ventircle via cerebral aqueduct (of Sylvius)
  • From fourth ventricle to subarachnoid space via Foramina of Luschka (Lateral) and foramen of Magendie (Medial)
122
Q

Communicating hydrocephalus

A
  • Decreased CSF absorption by archnoid granulations
  • Can lead to increased to increased intracranial pressure, papilledema, and herniation
  • e.g., arachnoid scarring post-meningitis
123
Q

Normal pressure hydrocephalus

A
  • Usually idiopathic
  • Results in increased subarachnoid space volume but no increase in CSF pressure
  • Expansion of ventricles distorts the fibers of the corona radiata, leading to the clinical triad of urinary incontinence, ataxia, and cognitive dysfunction (sometimes reversible)
  • {Wet, wobbly, wacky}
  • Improved by lumbar puncture, ventriculoperitoneal shunting
124
Q

Hydrocephalus ex vacuo

A
  • Apparent increase in CSF as the result of decreased neuronal tissue due to neuronal atrophy
  • Causes: Alzheimer’s, HIV, Pick’s disease, etc.
  • Intracranial pressure is normal; triad is not seen
125
Q

Noncommunicating hydrocephalus

A

Caused by a structural blockage of CSF circulation within the ventricular system (e.g., stenosis of the aqueduct of Sylvius)

126
Q

Number and locations of spinal nerves

A
  • 31 spinal nerves: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal
  • C1-C7 exit above corresponding vertebra; all others exit below
127
Q

Vertebral disc herniation

A
  • Nucleus pulposus (soft central disc) herniates through anulus fibrosus
  • Usually occurs posterolaterally at L4-L5 or L5-S1
128
Q

Lower extent of the spinal cord

A
  • In adults, it extends to the lower border of L1-L2 vergebrae (lower in infants)
  • Subarachnoid space (and its CSF) extends to the lower border of S2 vertebra
  • Lumbar punccture is isually performed between L3-L4 or L4-L5 (level of cauda equina)
129
Q

Extent of intermediate horn

A

T1 to L2/L3

130
Q

Organization of Dorsal columns

A
  • Fasciculus cuneatus (upper body, extremitis) is lateral
  • Fasciculus gracilis (lower body, extremities) is medial
  • {Dorsal column is organized as you are, with arms outside and legs inside}
131
Q

Organization of Lateral corticospinal tract

A
  • Legs are leteral
  • Arms are medial
  • {Legs are Lateral in Lateral corticospinal and spinothalamic tracts}
132
Q

Organization of anterior spinothalamic tract

A
  • Sacral is lateral
  • Cervical is medial
  • {Legs are Lateral in Lateral corticospinal and spinothalamic tracts}
133
Q

Function and organization of Dorsal-column/medial-lemniscal pathway

A

• Carries ascending pressure, vibration, fine touch, and proprioception information

  1. First order neuron has sensory nerve ending; cell body is in dorsal root ganglion; it enters the spinal cord and ascends ipsilaterally in dorsal column
  2. Synapse 1: ipsilateral nucleus cuneatus or gracilis in medulla
  3. second order neuron: decussates in medulla and ascends contralaterally in medial lemniscus
  4. Synapse 2: VPL of thalamus
  5. third order neuron in sensory cortex
134
Q

Function and organization of Spinothalamic tract

A

• Lateral: carries pain and temperature
• Anterior: carries crude touch, pressure
1. first order neuron has sensory nerve ending (A-delta and C fibers); cell body In dorsal root ganglion; enters spinal cord and ascends 2-3 segments ipsilaterally through dorsolateral tract of Lissauer
2. Synapse 1: ipsilateral gray matter in spinal cord
3. second order neuron: decussates at anterior white commissure and ascends contralaterally
4. Synapse 2: VPL of thalamus
5: third order neuron is in sensory cortex

135
Q

Function and organization of lateral corticospinal tract

A

• Carries descending voluntary movement of contralateral limbs

  1. Upper motor nuron: cell body in primary motor cortex; descends ipsilaterally through internal capsule until decussating at caudal medulla (pyramidal decussation); descends contralaterally
  2. Synapse at anterior horn of spinal cord
  3. Lower motor neuron leaves the spinal cord and synapses at the neuromuscular junction
136
Q

Signs of upper motor neuron lesion

A
  • Weakness
  • hyperreflexivity
  • increased tone
  • positive babinski sign (upwards)
  • Spastic paralysis
  • Clasp knife spasticity
  • {Upper MN = everything goes up (tone, DTR, toes)
137
Q

Signs of lower motor neuron lesion

A
  • Weakness
  • Atrophy
  • Fasciulations (muscle twitching)
  • decreased reflexes
  • Decreased tone
  • Flaccid paralysis
  • {Lower MN = everything lowered (muscle mass, tone, reflexes, downgoing toes)
138
Q

Spinal cord lesions in Poliomyelitsi and Werdnig-Hoffman disease

A
  • Due to destruction of anterior horns
  • LMN lesions only
  • Lead to flaccid paralysis
139
Q

Spinal cord lesions in multiple sclerosis

A
  • Random and asymmetric lesions due to demyelination
  • mostly white matter lesions of cervical region
  • Leads to scanning speech, intention tremor, nystagmus
140
Q

Spinal cord lesions in amyotrophic lateral sclerosis (ALS)

A
  • Combined UMN and LMN deficits with no sensory, cognitive, or oculomotor deficits
  • Both UMN and LMN lesion signs
  • Can be caused by defect in superoxide dismutase 1
  • Commonly presents as fasciculations with eventual atrophy
  • Progressive and fatal
  • Riluzole treatment modestly increases survival by decreasing presynaptic glutamase release
  • Lou Gehrig, Stephen Hawking
141
Q

Spincal cord lesions in complete occlusion of anterior spinal artery

A
  • Spares dorsal columns and Lissauer’s tract (pain and temperature fibers that ascend/descend 1-2 segments before penetrating gray matter)
  • Upper thoracic ASA terirtory is a watershed area, as artery of Adamkiewicz supplies ASA below T8
142
Q

Spinal cord lesions in Tabes dorsalis

A
  • Caused by tertiary syphilis
  • Results from degeneration (demyelination) of dorsal coloumns and roots
  • Leads to impaired sensation and proprioception as well as progressive sensorya taxia (inability to sense or feel the elgs)
  • Associated with Charcot’s joints, shooting pain, Argyll Robertson pupils (acommodation but no reaction)
  • Exam will demonstrate abscence of DTR and positive romberg sign (stand up, close eyes, and try to maintain balance)
143
Q

Spinal cord lesions in Syringomyelia

A
  • Syrinx (pseudocyst of CSF in spinal cord) expands and damages anterior white comissure of spinothalamic tract (second order neurons)
  • Leads to bilateral loss of pain and temperature sensation
  • usually occurs at C8-T1
  • Seen with Chiari I malformation
  • Can expand and affect other tracts
144
Q

Spinal cord lesions in Vitamin B12 or Vitamin E deficiency

A
  • Subacute combined degeneration: demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts
  • Leads to ataxic gait, paresthesia, impaired position sense, and impaired virbation sense
145
Q

Poliomyelitis

A
  • Caused by poliovirus (fecal-oral transmission)
  • Replicates in the oropharynx and small intestine before spreading via the bloodstream to the CNS
  • Infection causes destruction of cells in anterior horn of spinal cord (LMN death)
  • Symptoms:
    • LMN lesion signs - weakness, hypotonia, flaccid paralysis, atrophy, fasciculations, hyporeflexia, and muscle atrophy
    • signs of infection - malaise, headache, fever, mausea
  • Findings:
    • CSF with increased WBCs
    • CSF slight elevation of protein
    • no change in CSF glucose
    • Virus recovered from stool or throat
146
Q

Werdnig-Hoffman disease

A
  • Autosomal recessive inheritance
  • Congenital degeneration of anterior horns of spinal cord, leading to LMN lesion
  • Presentation: “Floppy baby” with marked hypotonia and tongue fasciculations
  • Infantile type has median age of death of 7 months
147
Q

Friedreich’s ataxia

A
  • Autosomal-recessive trinucleotide repeat disorder (GAA) in gene that encodes frataxin
  • Leads to impairment in mitochondiral functioning
  • Findings: Staggering gait, frequent fallig, nystagmus, dysarthria, pes cavus (high foot arches), hammer toes, hypertrophic cardiomyopathy (cause of death)
  • Presents in childhood with kyphoscoliosis
  • {Friedrich is fratastic (frataxin); he’s your favorite frat brother–always stumbling, staggering, and falling}
148
Q

Brown-sequard syndrome

A
  • Hemisection of spinal cord
  • Ipsilateral UMN signs below the level of the lesoin (due to corticospinal tract damage)
  • Ipsilateral LMN signs at the level of the lesion
  • Ipsilateral loss of tactile, vibration, porprioception sense below and at the level of the lesion (due to dorsal column damage)
  • Contralateral pain and temperature loss below the level of the lesion (due to spinothalamic tract damage)
  • Ipsiilateral pain and temperature loss at the level of the lesion (due to damage of the dorsolateral tract of lissauer)
  • If lesion occurs above T1, patient may present with Horner’s syndrome due to damage of sympathetic ganglion
149
Q

Horner’s syndrome

A
  • Associated with lesion of spinal cord above T1 (therefore damaging T1)
  • examples: Pancoast tumor, Brown-Sequard syndrome, late-stage syringomyelia
  • Findings are due to sympathectomy of face:
    • Ptosis: slight drooping of eyelid due to inaction of superior tarsal muscle
    • Anhidrosis: absence of sweating; flushing (rubor) of affected side
    • Miosis: pupil constriction
    • {PAM is horny}
150
Q

Oculosympathetic pathway

A
  1. First neuron projects from hypothalamus to the intermediolateral column of the spinal cord
  2. second neuron then goes to the superior cervical (sympathetic ganglion)
  3. The third neuron projects to the pupil, smooth muscle of eyelids, and sweat glands of the foreehad and face
    • Horner’s syndrome result from interruption of any of these pathways
151
Q

Landmark dermatomes

A
  • C2: posterior half of a skull cap
  • C3: high turtleneck shirt
  • C4: Low-collar shirt
  • T4: at the nipple {T4 at the teat pore}
  • T7: at the xiphoid process
  • T10: at the umbilicus (important for early appendicitis pain referral) {T10 at the belly butten}
  • L1: at the inguinal ligament {L1 is IL (inguinal Ligament)}
  • L4: includes the kneecaps {Down on aLl 4’s (L4)}
  • S2, S3, S4: erection and sensation of penile and anal zones {S2, S3, S4 keep the penis off the floor”
152
Q

Nerve tested by biceps reflex

A

C5 nerve root

153
Q

Nerve tested by Triceps reflex

A

C7 nerve root

154
Q

Nerve tested by patellar reflex

A

L4 nerve root

155
Q

Nerve tested by Achilles reflex

A

S1 nerve root

156
Q

Primitive reflexes

A
  • CNS reflexes that are present in a healthy infant but are absent in a neurologically intact adult
  • Normally disappear within first year of life
  • These primitive reflexes are inhibite dby a mature/developing frontal lobe
  • They may reemerge in adults following frontal lobe lesions
  • Moro reflex, rooting reflex, sucking reflex, palmar reflex, plantar reflex, galant reflex
157
Q

Moro reflex

A
  • Primitive reflex

* “hang on for life”: abduct/extend limbs when starteled, and then draw together

158
Q

Rooting reflex

A
  • Primitive reflex

* Movement of head toward one side if cheeck or mouth is stroked (nipple seeking)

159
Q

Sucking reflex

A
  • Primitive reflex

* Sucking response when roof of mouth is touched

160
Q

Palmar reflex

A
  • Primitive reflex

* Curling of fingers if palm is stroked

161
Q

Plantar reflex/Babinski sign

A
  • Primitive reflex
  • Dorsiflexion of large toe and fanning of other toes with plantar stimulation
  • Babinski sign - presence of this reflex in an adult, which may signify a UMN lesion
162
Q

Galant reflex

A
  • Primitive reflex
  • Stroking along one side of the spine while newborn is in ventral suspension (face down) causes lateral flexion of lower body toward stimulated side
163
Q

Cranial nerves that lie medially at brainstem

A
  • III, VI, XII
  • {Motor = medial}
  • {32=62=12}
164
Q

Cranial nerve that arises dorsally

A

CN IV arises dorsally and immediately decussates

165
Q

Function of Pineal gland

A

Melatonin secretion, circadian rhythms

166
Q

Function of superior colliculi

A

Conjugate vertical gaze center {Eyes are above ears - superior colliculus is visual; inferior colliculus is auditory}

167
Q

Function of inferior colliculi

A

Auditory {Eyes are above ears - superior colliculus is visual; inferior colliculus is auditory}

168
Q

Parinaud syndrome

A

Paralysis of conjugate vertical gaze due to lesion in superior colliculi (e.g., pinealoma)

169
Q

CN I - Olfactory

A
  • sensory: smell

* Only CN without thalamic relay to cortex

170
Q

CN II - Optic

A

Sensory: sight

171
Q

CN III - Oculomotor

A
  • Motor:
    • eye movements (SR, IR, MR, IO)
    • pupillary constriction (sphincter pupillae: Edinger-Westphal nucleus, muscarinic receptors)
    • Accomodation
    • Eyelid opening (levator palpebrae)
172
Q

CN IV - Trochlear

A

Motor: eye movement (SO)

173
Q

CN V - Trigeminal

A
  • Motor: Mastication
  • Sensory:
    • Facial sensation (ophthalmic, maxillary, mandibular divisions)
    • Somatosensation from anterior 2/3 of tongue
174
Q

CN VI - Abducens

A

Motor: Eye movement (LR)

175
Q

CN VII - Facial

A
  • Motor:
    • Facial movement
    • eyelid closing (orbicularis oculi)
  • Sensory:
    • Tase from anterior 2/3 of tongue
    • Stapedius muscle in ear (dampens vibrations of stapes, primairily to own voice)
  • Secretory:
    • Lacrimation
    • Salivation (submandibular and sublingual glands)
176
Q

CN VIII - Vestibulocochler

A
  • Sensory:
    • Hearing
    • Balance
177
Q

CN IX - Glossopharyngeal

A
  • Motor:
    • Stylopharyngeus (elevates pharynx, larynx)
    • Swallowing
  • Sensory:
    • Taste and somatosensation from posterior 1/3 of tongue
    • Monitoring carotid body and sinus chemo- and baroreceptors
  • Secretory: Salivation
178
Q

CN X - Vagus

A
  • Motor:
    • Swallowing
    • Palate elevation
    • Midline uvula
    • Talking
    • Coughing
  • Sensory:
    • Taste from epiglottic region
    • Thoracoabdominal viscera
    • Monitoring aortic arch chemo- and baroreceptors
179
Q

CN XI - Accessory

A
  • Motor:
    • Head turning (SCM)
    • Shoulder shrugging (Trapezius)
180
Q

CN XII - Hypoglossal

A

Motor: tongue movement

181
Q

Cranial nerve nuclei located in the tegmentum of the midbrain

A
  • III

* IV

182
Q

Cranial nerve nuclei located in the tegmentum of the pons

A
  • V
  • VI
  • VII
  • VIII
183
Q

Cranial nerve nuclei located in the tegmentum of the medulla

A
  • IX
  • X
  • XII
184
Q

Cranial nerve nuclei located in the tegmentum of the spinal cord

A

XI

185
Q

Sulcus limitans

A

Separates the cranial nerve motor nuclei (derived from the basal plate), from the cranial nerve sensory nuclei (derived from the alar plate) {Lateral - aLar; Medial - Motor}

186
Q

Corneal reflex pathway

A
  • Afferent: V-1 ophthalmic (nasociliary branch)

* Efferent: VII (temporal branch: orbicularis occuli)

187
Q

Lacrimation reflex pathway

A
  • Afferent: V-1
  • Efferent: VII
  • loss of reflex does not preclude emotional tears
188
Q

Jaw Jerk reflex pathway

A
  • Afferent: V-3 (muscle spindle from masseter)

* Efferent: V-3 (masseter)

189
Q

Pupillary reflex pathway

A
  • Afferent: II

* Efferent: III

190
Q

Gag reflex pathway

A
  • Afferent: IX

* Efferent: X

191
Q

Nucleus solitarius

A
  • Visceral sensory information: taste, baroreceptors, gut distention, etc
  • CN VII, IX, X
192
Q

Nucleus ambiguus

A
  • Motor innervation of pharynx, larynx, and upper esophagus: swallowing, palate elevation
  • CN IX, X
193
Q

Dorsal motor nucleus

A
  • Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI
  • CN X
194
Q

Structures exiting through cribriform plate

A

CN I

195
Q

Structures exiting through opitical canal (sphenoid bone)

A
  • CN II
  • Ophthalmic artery
  • Central retinal vein
196
Q

Structures exiting through superior orbital fissure (sphenoid bone)

A
  • CN III
  • CN IV
  • CN V-1 {Divisions of CN V exit owing to Standing Room Only}
  • CN VI
  • Ophthalmic vein
  • Sympathetic fibers
197
Q

Structures exiting through foramen Rotundum (sphenoid bone)

A

CN V-2 {Divisions of CN V exit owing to Standing Room Only}

198
Q

Structures exiting through foramen Ovale

A

CN V-3 {Divisions of CN V exit owing to Standing Room Only}

199
Q

Structures exiting through foramen spinosum

A

Middle meningeal artery

200
Q

Structures exiting through Internal auditory meatus

A
  • CN VII

* CN VIII

201
Q

Structures exiting through Jugular foramen

A
  • CN IX
  • CN X
  • CN XI
  • Jugular vein
202
Q

Structures exiting through hypoglossal canal

A

• CN XII

203
Q

Structures exiting through foramen magnum

A
  • Spinal roots of CN XI
  • Brain stem
  • Vertebral arteries
204
Q

Structures passing through cavernous sinus

A
  • sinuses on either side of the pituitary; empty into the IJV
  • CN III, IV, VI
  • CN V-1, V-2
  • Postganglionic sympathetic fibers en route to the orbit
205
Q

Cavernous sinus syndrome

A
  • Ophthalmoplegia and decreased corneal and maxillary sensation with normal vision
  • Caused by mass effect, fistula, thrombosis
206
Q

Presentation of CN V motor lesion

A

Jaw defiates toward side of lesion due to unopposed force from the opposite pterygoid (innervated by CN V)

207
Q

Presentation of CN X lesion

A

Uvula deviates away from side of lesion and weak side collapses

208
Q

Presentation of CN XI lesion

A
  • Weakness turning head to contralateral side of lesion (SCM contracts to turn head to contralateral side)
  • Shoulder droop on side of lesion (trapezius
209
Q

Presentation of CN XII lesion(LMN)

A

Tongue deviates toward side of lesion due to weakened tongue muscles on the afffected side {lick your wounds}

210
Q

Examination of conductive hearing loss

A
  • Rinne test: abnormal (bone > air)

* Weber test: localilzes to affected ear

211
Q

Examination of sensorineural hearing loss

A
  • Rinne test: normal (air > bone)

* Weber test: localizes to unaffected ear

212
Q

Noise-induced hearing loss

A
  • Damage to sterociliated cells in organ of Corti
    • Loss of high-frequency hearing first
  • Sudden extremely-loud noises can produce hearing loss due to tympanic membrane rupture
213
Q

Facial lesions

A
  • Cortical inputs go to upper and lower divisions of facial nucleus
    • Forehead LMN receive bilateral UMN input
    • Lower face LMN receive contralateral UMN input
  • LMN injury affects ipsilateral side of face (forehead and lower face)
  • UMN injury affects contralateral lower face
214
Q

Facial nerve palsy

A
  • Complete destruction of the facial nucleus or its branchial efferent fibers
  • Leads to peripheral ipsilateral facial paralysis with inability to close eye on involved side
  • Can be seen as a complication in AIDS, Lyme disease, herpes simplex and (less commonly) herpes zoster, sarcoidosis, tumors, and diabetes
  • Bell’s palsy: facial nerve palsy can occur idiopathically; most of these cases lead to gradual recovery
215
Q

Muscles of mastication

A
  • All are innervated by the mandibular branch of the trigeminal nerve (V-3)
  • 3 muscles close the jaw {M’s Munch; “it takes more muscle to keep your mouth shut”}
    • Masseter
    • TeMporalis
    • Medial pterygoid
  • 1 muscle opens the jaw: Lateral pterygoid {Lateral Lowers}
216
Q

Refractive eye errors

A

Impaired vision that improves with glasses

217
Q

Hyperopia

A
  • Refractive error
  • eye too short for refracctive power of cornea and lens, leads to light focusing behind the retina
  • can’t see close objects
218
Q

Myopia

A
  • Refractive error
  • Eye too long for refractive power of cornea and lesn, light focuses in front of retina
  • can’t see objects far away
219
Q

Astigmatism

A
  • Refractive error

* Abnormal curvature of cornea results in different refractive power at different axes

220
Q

Accomodation

A
  • Focusing on near objects
  • Ciliary muscles tighten, zonula fibers relax, and lens becomes more convex
  • Occurs along with convergence and miosis
221
Q

Presbyopia

A
  • refractive error
  • Decreased change in focusing ability during accommodation due to sclerosis and decreased elasticity
  • Patients have trouble seeing nearby objects
  • Age-related
222
Q

Uveitis

A
  • Inflammation of uveal coat (iris, ciliary body, choroid)
  • Often associated with systemic inflammation disorders: sarcoid, rheumatoid arthritis, juvenile idiopathic arthritis, TB, HLA-B27-associated conditions (seronegative spondylarthropathis), etc
223
Q

Retinitis

A
  • Retinal edema and necrosis leading to scar
  • Often viral (CMV, HSV, HZV)
  • Associated with immunosuprresion
224
Q

Central retinal artery occlusion

A
  • Acute, painless monocular vision loss

* Leads to retina whitening with cherry-red spot

225
Q

Aqueous humor pathway

A
  1. Ciliary epithelium produces aqueous humor
  2. aqueous humor passes from posterior chamber to anterior chamber through the pupil the lens and the iris
  3. Trabecular meshwork collects aqueous humor that flows through anterior chamber
  4. Canal of Schlemm collects aqueous humor from trabecular meshwork
226
Q

Receptors in ciliary muscle

A

Muscarinic ACh

227
Q

Receptors in ciliary epithelium

A

beta adrenergic

228
Q

Receptors in pupillary dilator muscle of Iris

A

alpha-1 adrenergic

229
Q

Receptors in pupillary sphincter muscle of iris

A

M3 ACh

230
Q

Glaucoma

A
  • Optic neuropathy, usually with increased intraocular pressure (IOP)
  • Two main types
    • Open/wide angle type
    • Closed/narrow angle type
231
Q

Open/wide angle glaucoma

A
  • Characterized by peripheral then central vision loss, usually with increased intraocular pressure; painless
  • Optic disc atrophy with cupping
  • Associated with: age, African-American race, family history, increased intraocular pressure
  • More common in the US
  • Primary cause unclear
  • Secondary causes: uveitis, trauma, corticosteroids, vasoproliferative retinopaty that can block or decrease outflow at the trabecular meshwork
232
Q

Closed/narrow angle glaucoma

A
  • Enlargement or forward movement of lens against central iris leads to obstruction of normal aqueous flow through pupil, this leads to fluid build up behind iris, which pushes the peripheral iris against corena and impeding flow through the trabecular meshwork
  • Chronic closure: often asymptomatic, whith damage to optic nerve and peripheral vision
  • Acute closure: True ophthalmic emergency: increased IOP pushed iris forward, leading to abrupt closure of the angle
    • Very painful, sudden vision loss, halos around lights, rock-hard eye, frontal headache
    • Do not give epinephrine becacuse of its mydriatic effect (which leads to further closure of trabecular network)
233
Q

Cataract

A
  • Painless, often bilateral opacification of lens, leading to a decrease I vision
  • Risk factors:
    • Age
    • Smoking
    • EtOH
    • Excessive sunlight
    • Prolonged corticosteroid use
    • Classic galatosemia
    • Galactokinase deficiency
    • Diabetes (sorbitol)
    • Trauma
    • Infection
234
Q

Papilledema

A
  • Optic disc swelling (usually bilateral) due to increased intracraneal pressure (usually secondary to mass effect)
  • presentation: enlarged blind spot and elevated optic disc with blurred margings seen on fundoscopic exam
235
Q

Extraocular muscle innervation

A
  • CN VI innervates the Lateral Rectus
  • CN IV innervates the Superior Oblique (abducts, intorts, and depresses while aducted)
  • CN II innervates the Rest (superior rectus, medial rectus, inferior rectus, inferior oblique)
  • {LR6SO4R3}
236
Q

Effect on extraocular movements of CN III damage

A
  • Eye look sdown and out

* Ptosis, pupillary dilation, loss of accommodation

237
Q

Effect on extraocular movements of CN IV damage

A

Eye moves upward, particularly with contralateral gaze and ipsilateral head tilt (problems going downstairs)

238
Q

Effect on extraocular movements of CN VI damage

A

Medially directed eye that cannot abduct

239
Q

Testing extraocular muscles

A
  • lateral rectus: laterally
  • Medial rectus: medially
  • Superior rectus: laterally and up
  • Inferior rectus: laterally and down
  • Superior oblique: medially and down
  • Inferior obliqe: medially and up
240
Q

Pathway for pupillary miosis (constriction)

A

• Parasympathetic

  1. first neuron: edinger-Westphal nucleus to ciliar ganglion via CN III
  2. second neron: short ciliary nerves to pupillary sphincter muscles
241
Q

Pathway for pupillary mydriasis (dilation)

A

• Sympathetic

  1. first neuron: hypothalamus to ciliospinal center of Budge (C8-T2)
  2. second neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels)
  3. third neuron: plexus along internal carotid, through cavernous sinus; enters orbit as long ciliary nerve to pupillary dilator muscles
242
Q

Pathway of pupillary light reflex

A
  1. Light in either retina sends a signal via CN II to pretectal nuclei in midbrain
  2. pretectal nuclei activate bilateral Edinger-Westphal nuclei
  3. Both pupils contract bilaterally through action of CN III
243
Q

Marcus Gunn pupil

A
  • Afferent pupillary defect (e.g., due to optic nerve damage or retinal detachment)
  • Leads to decreased bilateral pupillary constriction when light is shone in affected eye relative to the unaffected eye
  • Tested with the swinging flashlight test
244
Q

Arrangement of nerve fibers on CN III

A
  • CN III motor components are centrally located on the nerve
  • Motor output to ocular muscle is affected primarily by vascular disease (e.g., diabetes: glucose to sorbitol) due to decreased diffusion of oxygen and nutrients to the interior fibers from compromised vasculature outside of nerve
    • Signs: Ptosis, “down and out” gaze
  • CN III parasympathetic components are peripherally located on the nerve
  • Fibers on the periphery are the first affected by compression (e.g., Pcomm aneurysm uncal herniation)
    • Signs: diminished or absent pupillary light reflex, “blown” pupil
245
Q

Arrangement of retina

A
  • From outer to inner layer:
  • Pigment cell: shield excess light, supports retina
  • Photoreceptor (rods or cones)
  • bipolar cell
  • ganglion cell
246
Q

Rods

A
  • Photoreceptors
  • Have long, cylindrical outer segment
  • Pigment is rhodopsin
  • Very sensitive to low light levels: vision at night with no color differentiation
  • More on the periphery of retina
247
Q

Cones

A
  • Photoreceptors
  • Have shorter tapered outer segments
  • 3 different pigments (for red, green, blue): Bright light vision with color differentiation
  • More toward center of retina
248
Q

Retinal detachment

A
  • Separation of neurosensory layer of retina (photoreceptors) from outermost pigmented epithelium, leading to degeneration of photoreceptors and vision loss
  • May be secondary to retinal breaks, diabetic traction, inflammatory effusions
  • Breaks are more common in patients with high myopia
  • Are often preceded by posterior vitreus detachment (flashes and floaters)
  • Lead to a monocular loss of vision like a “curtain drawn down”
  • Surgical emergency
249
Q

Age-related macular degeneration

A
  • Degeneration of macula (central area of retina)
  • Causes distortion (metamorphosia) and eventual loss of central vision (scotomas)
  • Dry (nonexudative):
    • > 80 % of cases
    • Due to deposition of yellowish extracellular material beneath retinal pigment epithelium (drusen) with gradual loss of vision
    • Prevent progression with multivitamin and antioxidant supplements
  • Weat (exudative):
    • 10-15% of cases
    • Rapid loss of vision due to bleeding secondary to choroidal neovascularization
    • Treat with anti-vascular endothelial growth factor injections (anti-VEGF) or laser
250
Q

Meyer’s loop

A
  • Projections from lateral geniculate body to lower bank of calcarine sulcus
  • Loop around inferior horn of lateral ventricle (temporal lobe)
  • upper contralateral quadrants of visual field
251
Q

Dorsal optic radiations

A
  • Projections from lateral geniculate body to upper bank of calcarine sulcus
  • Go through internal capsule (parietal lobe)
  • lower contralateral quadrants of visual field
252
Q

Visual defect resulting from lesion of optic nerve

A

Ipsilateral anopia

253
Q

Visual defect resulting from lesion of optic chiasm

A

Bitemporal hemianopsia

254
Q

Visual defect resulting from lesion of Optic tract

A

Contralateral homonymous hemianopsia

255
Q

Visual defect resulting from lesion of Meyer’s loop (temporal lobe)

A
  • contralateral upper quadrantanopsia (not macular sparing if complete lesion)
  • e.g.: temporal lesion, MCA
256
Q

Visual defect resulting from lesion of Dorsal optic radiations (parietal lobe)

A
  • contralateral lower quadrantanopsia (not macular sparing if complete lesion)
  • e.g.: parietal lesion, MCA
257
Q

Visual defect resulting from diffusion lesion of calcarine sulcus

A
  • Contralateral hemianopsia with macular sparing

* e.g.: PCA infarct

258
Q

Visual defect resulting from lesion of macula

A
  • Central scotoma

* e.g.: due to macular degeneration

259
Q

Medial longitudinal fasciculus (MLF)

A
  • Pair of tracts that allow for crosstalk between nuclei of CN VI and CN III to coordinate both eyes to move in same horizontal direction
  • Nucleus of VI projects to contralateral MLF to activate contralateral CN III to activate contralateral medial rectus
  • Highly myelinated (must communicate quickly so eyes move at same time)
  • Lesions seen in pateitns with demyelination
260
Q

Internuclear ophthalmoplegia (MLF syndrome)

A
  • Lesion in MLF
  • Lack of communicaation so that CN VI activates ipsilateral LR but does not lead toa ctivation of contralateral MR
  • Abducting eye gets nystagmus (CN VI overfires to stimulate Cn III)
  • Convergence is normal

FA13 Neurology (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions