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Neuro Exam 2 - JLJ > Clinical > Flashcards

Clinical Flashcards

1
Q

Disclaimer: I was very tired when I made these flash cards, so I may have missed some clinical notes that were covered in class but not listed in here. Also, this deck only includes clinical notes that we specifically covered in lecture, not necessarily what deficits will you have if a lesion occurs here, what tracts are affected, etc.

A

Feel free to add to this deck or let me know if something is missing and I can add it.

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2
Q

What is vertebral basilar insufficiency?

A

Reduced blood flow from the vertebral arteries that occurs during extreme hyperextension of the head or during extreme head rotation (this is also known as Bow-Hunter’s Syndrome)

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3
Q

What is subclavian steal syndrome?

A

Occurs when the subclavian artery steals blood from the contralateral vertebral artery and shunts the blood to the UE

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4
Q

What is a subfalcine (cingulate, falcine, falx) herniation?

A

Occurs in supratentorial compartment; displaces brain tissue under the falx cerebri; may compress anterior cerebral artery, frontal lobe, parietal lobe; may evolve into a transtentorial herniation

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5
Q

What is a transtentorial (central) herniation?

A

Brain is displaced downward toward tentorial notch; compromises the upper brainstem, CN III, and possibly lower structures; may also compress basilar artery and posterior cerebral arteries; results in decorticate and decerebrate rigidity

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6
Q

What is a uncal herniation?

A

Uncus and usually portions of parahippocampal gyrus are extruded over the edge of tentorium cerebelli and through the tentorial notch; impinges on the brain

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7
Q

What is a tonsilar herniation?

A

Herniation of cerebellar tonsils through the foramen magnum; leads to compression of the medulla and upper cervical spinal cord

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8
Q

In a epidural hematoma, where does it bleed into? What is the common site this occurs? What is the source of the bleeding? What are the clinical signs? What is the treatment?

A

Bleeds Into: epidural space between skull and dura mater

Common Site: fracture of squamous temporal bone or pterion

Source: middle meningeal artery

Signs: momentary unconsciousness followed by lucid period of hours to 1-2 days then unconsciousness

Treatment: surgical

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9
Q

In a subdural hematoma, where does it bleed into? What is the occurrence that causes this to happen? What is the source of the bleeding? What are the clinical signs? What is the treatment?

A

Bleeds Into: between dura and arachnoid mater

Occurrence: head strikes fixed object or during an assault

Source: venous, usually cortical veins opening into superior sagittal sinus

Signs: slower accumulation of blood due to pressure and often self-limiting

Treatment: surgical

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10
Q

For a subarachnoid hemorrhage, when is this commonly found? What is the source of the bleeding? What are the clinical signs?

A

Commonly Found: severe head injury, but more common in rupture of aneurysm

Source: arterial bleeding from cerebral arteries

Signs: massive bleeding into CSF compartment due to arterial source with headaches and deteriorating level of consciousness

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11
Q

What is a intracerebral (subpial) hemorrhage? What is the source? What are the clinical signs?

A

Bleeding within brain substance (stroke); can be a complication in 2-3% of all head injuries

Source: middle cerebral artery

Signs: hypertension or degenerative arterial disease (commonly seen at autopsy

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12
Q

What are the symptoms of Alzheimer’s?

A

Memory failure, progressing steadily to involve motor skills, speech, and sensation

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13
Q

What are the clinical features of Parkinson’s?

A

Tremor, slow movement, and rigidity resulting from degeneration of neurons in the substantia nigra, which leads to a loss of dopamine

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14
Q

What are some things associated with Parkinson’s?

A

Lewy bodies and alpha-synuclein proteins

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15
Q

What are some things associated with Alzheimer’s?

A

Amyloid beta plaques and neurofibrillary tangles

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16
Q

What is the most common neurodegenerative disease?

A

Alzheimer’s

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17
Q

What is aqueductal stenosis? Communicating/non-communicating? Obstructive/non-obstructive?

A

Accumulation of CSF in the lateral and third ventricles due to obstruction; it is non-communicating and obstructive

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18
Q

What are the causes of aqueductal stenosis?

A

Congenital, most common, can be x-linked; tumor, pineal gland; previous case of meningitis leading to scarring or other infection; inflammation from intrauterine infection

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19
Q

What is normal pressure hydrocephalus?

A

CSF fails to drain properly leading to enlarged ventricles and cortical atrophy; it is a form of communicating hydrocephalus

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20
Q

What is normal pressure hydrocephalus caused by? What is the “TRIAD”?

A

Caused by increased CSF viscosity, altered elasticity of ventricular walls, or impaired CSF absorption

TRIAD: cognitive impairment/confusion (wacky), unsteady, magnetic gait (wobbly), and urinary incontinence (wet)

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21
Q

What is the Dandy-Walker Malformation? Communicating/non-communicating? Obstructive/non-obstructive?

A

It is a congenital brain malformation where fluid accumulates in the 4th ventricle; it is obstructive and non-communicating

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22
Q

What causes Dandy-Walker malformation?

A

4th ventricle outlet obstruction (enlarged ventricle) and/or cerebellar hypoplasia, specifically partial or complete agenesis of vermis

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23
Q

What is Chiari II?

A

Downward displacement of inferior cerebellar vermis and tonsils through the foramen magnum; associated with lumbosacral myelomeningocele; form of non-communicating hydrocephalus; fluid accumulates above 4th ventricle

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24
Q

What are the treatments for Chiari II?

A

Most common treatment is a shunt that is placed so that fluid can drain to another part of the body; contains a valve that keeps the fluid flowing in the right direction and at the correct speed; most people will need this for the rest of their lives

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25
Q

What is holoprosencephaly?

A

Incomplete separation of the cerebral hemispheres caused by defects in forebrain development that often cause facial anomalies resulting from a reduction of the facial/frontal neuropore (FNP); leads to cyclopia, premaxillary agenesis, proboscis, single-nostril, hypotelorism, facial clefts

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26
Q

What is lissencephaly?

A

Incomplete neuronal migration to cerebral cortex during 3-4 months of gestation; smooth cerebral surface consisting of broad, thick gyri (pachygyria) or lack of gyri (agyria) and neuronal heterotopia (cells in aberrant positions compared to normal); enlarged ventricles and malformation of the corpus callosum are common; will initially appear normal but later develop seizures, profound mental deficiency, and mild spastic quadriplegia

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27
Q

What is microcephaly?

A

Neurodevelopmental disorder where calvaria and brain are small, but the face is normal size; significant mental deficiencies due to brain underdevelopment; results from a reduction in brain growth; caused by autosomal recessive primary microcephaly, ionizing radiation, infectious agents, and maternal alcohol abuse

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28
Q

What is sensory ataxia?

A

Loss of muscle stretch (tendon) reflexes, and proprioceptive losses from the extremities due to lack of sensory input; patient may also have wide-based stance and may place feet to the floor with force, in an effort to create the missing proprioceptive input

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29
Q

What is the jaw-jerk reflex?

A

Stretching the masseter (downward tap on chin), causes it to contract bilaterally; amplitude of the reflex is typically minor, but it is enhanced after UMN damage

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30
Q

What does Brown-Sequard syndrome cause contralaterally? Ipsilaterally?

A

Contra: loss of nociceptive and thermal sensations over body beginning about 2 segments below level of lesion (ALS damage)

Ipsil: loss of discriminative tactile, vibratory, and position sense over the body at and below the level of the lesion (posterior column damage); motor loss with paralysis of extremities (depending on level)

31
Q

What is syringomyelia?

A

Formation of cysts within the spinal cord; may impinge on anterior white commissure that contains decussating ALS fibers; resulting patter is shawl or cape; motor function is also lost; may have LMN signs if ventral horns affected, may have UMN signs if lateral corticospinal tract is affected

32
Q

What happens when syringomyelia occurs at C4-5?

A

Bilateral loss of nondiscriminative tactile, nociceptive, and thermal sensations; starts below lesion (several segements); “cape-like” distribution of loss over the shoulders and down to the nipple level

33
Q

What is a Herpes Zoster infection (shingles)?

A

Viral infection that reactivates when under stress; virions travel down peripheral processes of the neurons to produce skin irritation in the dermatome; leads to diminished sensibility (hypesthesia) over affected dermatomes with poorly understood pain (postherpetic neuralgia)

34
Q

What is medullary syndrome?

A

In medulla, ALS fibers are near anterolateral surface but remain separate from PCMLS through medulla and pons; vascular lesions or tumors in brainstem can affect discriminative touch and nociception differentially

35
Q

What is lateral medullary (wallenberg) syndrome?

A

Vascular lesion to PICA, which supplies territory of ALS and spinal trigeminal nucleus/tract; results in contralateral loss of pain and temp over body with ipsilateral loss of pain and temp over face

36
Q

What is alternating analgesia of trigeminal nerve?

A

Brainstem lesions in upper medulla destroy primary fibers in spinal trigeminal tract (descending tract of V) and secondary fibers in spinal lemniscus; patients demonstrate ipsilateral hemianalgesia of face and contralateral hemianalgesia of body

37
Q

What is alternating trigeminal hemiplegia?

A

Unilateral destruction of trigeminal nerve and CST(?) in pons; ipsilateral trigeminal anesthesia and paralysis; contralateral spastic hemiplegia

38
Q

What is Meniere’s Disease?

A

Disruption of normal endolymph volume, resulting in endolymphatic hydrops (abnormal distention of membranous labyrinth)

39
Q

What are the symptoms of Meniere’s?

A

Fluctuating hearing loss, vertigo, positional nystagmus, and nausea; also unpredictable attacks of auditory and vestibular symptoms, including vomiting, tinnitus, and inability to make head movements or even stand passively

40
Q

What are the treatments for Meniere’s?

A

Diuretic and salt restricted diet to reduce hydrops; implantation of a small shunt into swollen endolymphatic sac

41
Q

What is vertigo? Subjective vertigo? Objective vertigo?

A

Vertigo: illusion of body motion, often spinning or turning, experienced when no real motion is taking place

Subjective: patient experiences the sensation of spinning while things in the environment are not moving

Objective: sensation is one of objects spinning while patient is not moving

42
Q

What is benign paroxysomal positional vertigo?

A

Characterized by brief episodes of vertigo that coincide with particular changes in body position; triggered by turning over in bed, getting up in the morning, bending over, or rising from bent position

43
Q

What is a vestibular schwannoma?

A

Benign tumor that originates from schwann cells of the vestibular root (90% of cases and 5-10% of all intracranial tumors); typically found within cerebellopontine angle -> impinges on structures traversing internal acoustic meatus (VII, VIII, labyrinthine artery); slow growing

44
Q

What is vestibular neuritis? What are some treatments?

A

Thought to involve edema of the vestibular nerve/ganglion; patients present with severe vertigo, nausea, and vomiting, but no accompanying hearing loss or other CNS deficits

Treatments: antiemetics, vestibular suppressants, corticosteroids, and antiviral agents

45
Q

What is the vestibuloocular reflex?

A

When turning your head, your eyes turn the opposite direction; at this moment, the eyes are at the back of the orbit and can’t go back further; eyes intermittently and rapidly reset back to a central position

46
Q

What is the caloric test?

A

Tests vestibular labyrinth function/VOR (vestibuloocular reflex) without moving the head; uses water to alter convection currents in endolymph that alters CN VIII firing rate

47
Q

What does warm water cause in the caloric test?

A

Generates currents that mimic turning head to irrigated side; nystagmus that beats toward irrigated ear

48
Q

What does cold water cause in the caloric test?

A

Opposite effect of warm water; nystagmus that beats away from irrigated ear

49
Q

What is the oculocephalic reflex/head thrust test?

A

Rotating the head back and forth horizontally that induces compensatory eye movements that are dependent on visual and vestibular function; reflex occurs when eyes move in opposite direction of the head movements -> doll’s eyes

50
Q

What happens in conscious patients when testing the oculocephalic reflex? Comatose patients?

A

Conscious: doll’s eyes are absent due to voluntary eye movements that mask the reflex

Comatose: reflex is used to assess brainstem function; if the brainstem is intact the doll’s eye reflex is present; if brainstem contains a lesion, doll’s eye reflex is absent

51
Q

What is the Law of Projection?

A

States that regardless of the place along an afferent pathway that is stimulated, the sensation is perceived to come from the place that the innervation arises

52
Q

What is dysdiadochokinesia?

A

Inability to rapidly alternate movements

53
Q

What is dysmetria?

A

Inability to accurately move an intended distance

54
Q

What is an action tremor?

A

Shaking of the limb during voluntary movement

55
Q

What are the signs of a LMN lesion?

A

Flaccid paralysis, wasting or atrophy, hyporeflexia/areflexia due to denervation, hypotonia, denervation hypersensitivity, and fasciculations

56
Q

What are the signs of a UMN lesion?

A

Loss of distal extremity strength and dexterity, positive Babinski, pronator drip, hypertonia, spasticity, rigidity, hyperreflexia, and clasp-knife phenomenon (collapse of resistance at the end of the range of motion)

57
Q

What is decorticate posture?

A

Lesion above red nucleus (which is in the midbrain); thumb tucked under flexed fingers in fisted position, pronation of forearm, flexion at elbow with lower extremity in extension with foot inversion

58
Q

What is decerebrate posture?

A

Lesion below red nucleus but above reticulospinal and vestibulospinal nuclei; upper extremity in pronation and extension and lower extremity in extension

59
Q

What is anterior cord syndrome?

A

Compression or damage to anterior part of spinal cord; usually due to spinal cord infarction, intervertebral disc herniation, and radiation myelopathy

60
Q

What is central cord syndrome?

A

Compression and damage to central portion of spinal cord; mechanism of injury is usually cervical hyperextension

61
Q

What is central 7 palsy?

A

Lesion of corticobulbar tract involving CN VII; muscles of upper face are controlled bilaterally, while muscles of the lower face are controlled contralaterally

Note: lesion rostral to facial motor nucleus results in drooping of muscles at corner of the mouth on the side opposite the lesion

62
Q

What is Bell’s palsy?

A

Ipsilateral flaccid paralysis of upper and lower face

63
Q

What is spastic cerebral palsy?

A

Results from abnormal supraspinal influences, failure of normal neuronal selection, or consequent aberrant muscle development; causes paresis, abnormal tonic stretch reflexes, reflex irradiation, lack of postural preparation prior to movement, and abnormal cocontraction of muscles

64
Q

What is ALS (Lou Gehrig’s)?

A

Disease that destroys only somatic motor neurons, UMNs, brainstem, and spinal cord LMNs; leads to paresis, myoplastic hyperstiffness, hyperreflexia, Babinski’s sign, atrophy, fasciculations, and fibrillations; cranial nerve involvement leads to difficulty breathing, swallowing, and speaking

65
Q

What is polyneuropathy?

A

Involves sensory, motor, and autonomics; progresses from distal to proximal due to dying-back or impaired axonal transport; demyelization may also contribute

66
Q

What is Huntington’s Chorea?

A

Degeneration of neurons in striatum leading to decreased GABA

67
Q

What is Huntington’s Disease?

A

Progressive disease with average onset of 45; autosomal dominant HTT gene mutation with CAG repeats

68
Q

What are the characteristics of Huntington’s Disease?

A

Characterized by involuntary, jerky, rapid movements, dementia, unsteady gait, slurred speech, trouble maintaining tongue protrusion, irregular breathing, many patients also diagnosed with depression not just because of the illness; also higher risk of suicide

69
Q

What are the treatments for Huntington’s Disease?

A

Tetrabenazine (serotonin antagonist), typical antipsychotic (antagonize dopamine), or reserpine/tetrabenazine (depleting dopamine)

70
Q

What is Ballismus?

A

Flailing, flinging movement of the whole extremity seen in lesions of the contralateral subthalamic nucleus; can be related to stroke, inflammation, or tumor

71
Q

What is Chorea?

A

Spontaneous, rapid, jerky, arrhythmic, and involuntary movements which are purposeless or “fragments of motor programs”

72
Q

What are the symptoms of acute rheumatic fever (Jones criteria)?

A 
J - joints (arthritis)
O - heart (-carditis)
N - nodules (subcutaneous)
E - erythema marginatum
S - Sydenham's chorea
73
Q

What is athetosis?

A

Inability to sustain the body part in one position; movements are writing or snake-like; often seen with chorea; can be seen in combination with other disorders; seen with dopamine-blocking drugs or hypoxic-ischemic injury

74
Q

What is Writer’s Cramp (Focal Dystonia)?

A

Persistence or fixing of the posture at the extreme of an athetoid movement of either the extremities or the trunk; non-painful but can severely affect ability to write (even causing word to be illegible); involuntary, sustained muscle contracture of extensors and/or flexors of hand

Neuro Exam 2 - JLJ (16 decks)

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