Clinical

Question 1

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.

Answer 1

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

Question 2

What is vertebral basilar insufficiency?

Answer 2

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)

Question 3

What is subclavian steal syndrome?

Answer 3

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

Question 4

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

Answer 4

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

Question 5

What is a transtentorial (central) herniation?

Answer 5

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

Question 6

What is a uncal herniation?

Answer 6

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

Question 7

What is a tonsilar herniation?

Answer 7

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

Question 8

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?

Answer 8

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

Question 9

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?

Answer 9

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

Question 10

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

Answer 10

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

Question 11

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

Answer 11

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

Question 12

What are the symptoms of Alzheimer’s?

Answer 12

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

Question 13

What are the clinical features of Parkinson’s?

Answer 13

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

Question 14

What are some things associated with Parkinson’s?

Answer 14

Lewy bodies and alpha-synuclein proteins

Question 15

What are some things associated with Alzheimer’s?

Answer 15

Amyloid beta plaques and neurofibrillary tangles

Question 16

What is the most common neurodegenerative disease?

Answer 16

Alzheimer’s

Question 17

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

Answer 17

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

Question 18

What are the causes of aqueductal stenosis?

Answer 18

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

Question 19

What is normal pressure hydrocephalus?

Answer 19

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

Question 20

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

Answer 20

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)

Question 21

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

Answer 21

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

Question 22

What causes Dandy-Walker malformation?

Answer 22

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

Question 23

What is Chiari II?

Answer 23

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

Question 24

What are the treatments for Chiari II?

Answer 24

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

Question 25

What is holoprosencephaly?

Answer 25

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

Question 26

What is lissencephaly?

Answer 26

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

Question 27

What is microcephaly?

Answer 27

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

Question 28

What is sensory ataxia?

Answer 28

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

Question 29

What is the jaw-jerk reflex?

Answer 29

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

Question 30

What does Brown-Sequard syndrome cause contralaterally? Ipsilaterally?

Answer 30

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)

Question 31

What is syringomyelia?

Answer 31

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

Question 32

What happens when syringomyelia occurs at C4-5?

Answer 32

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

Question 33

What is a Herpes Zoster infection (shingles)?

Answer 33

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)

Question 34

What is medullary syndrome?

Answer 34

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

Question 35

What is lateral medullary (wallenberg) syndrome?

Answer 35

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

Question 36

What is alternating analgesia of trigeminal nerve?

Answer 36

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

Question 37

What is alternating trigeminal hemiplegia?

Answer 37

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

Question 38

What is Meniere's Disease?

Answer 38

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

Question 39

What are the symptoms of Meniere's?

Answer 39

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

Question 40

What are the treatments for Meniere's?

Answer 40

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

Question 41

What is vertigo? Subjective vertigo? Objective vertigo?

Answer 41

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

Question 42

What is benign paroxysomal positional vertigo?

Answer 42

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

Question 43

What is a vestibular schwannoma?

Answer 43

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

Question 44

What is vestibular neuritis? What are some treatments?

Answer 44

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

Question 45

What is the vestibuloocular reflex?

Answer 45

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

Question 46

What is the caloric test?

Answer 46

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

Question 47

What does warm water cause in the caloric test?

Answer 47

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

Question 48

What does cold water cause in the caloric test?

Answer 48

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

Question 49

What is the oculocephalic reflex/head thrust test?

Answer 49

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

Question 50

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

Answer 50

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

Question 51

What is the Law of Projection?

Answer 51

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

Question 52

What is dysdiadochokinesia?

Answer 52

Inability to rapidly alternate movements

Question 53

What is dysmetria?

Answer 53

Inability to accurately move an intended distance

Question 54

What is an action tremor?

Answer 54

Shaking of the limb during voluntary movement

Question 55

What are the signs of a LMN lesion?

Answer 55

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

Question 56

What are the signs of a UMN lesion?

Answer 56

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)

Question 57

What is decorticate posture?

Answer 57

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

Question 58

What is decerebrate posture?

Answer 58

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

Question 59

What is anterior cord syndrome?

Answer 59

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

Question 60

What is central cord syndrome?

Answer 60

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

Question 61

What is central 7 palsy?

Answer 61

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*

Question 62

What is Bell's palsy?

Answer 62

Ipsilateral flaccid paralysis of upper and lower face

Question 63

What is spastic cerebral palsy?

Answer 63

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

Question 64

What is ALS (Lou Gehrig's)?

Answer 64

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

Question 65

What is polyneuropathy?

Answer 65

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

Question 66

What is Huntington's Chorea?

Answer 66

Degeneration of neurons in striatum leading to decreased GABA

Question 67

What is Huntington's Disease?

Answer 67

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

Question 68

What are the characteristics of Huntington's Disease?

Answer 68

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

Question 69

What are the treatments for Huntington's Disease?

Answer 69

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

Question 70

What is Ballismus?

Answer 70

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

Question 71

What is Chorea?

Answer 71

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

Question 72

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

Answer 72

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

Question 73

What is athetosis?

Answer 73

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

Question 74

What is Writer's Cramp (Focal Dystonia)?

Answer 74

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