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Neuroscience BB Exam 3 > Motor Systems > Flashcards

Motor Systems Flashcards

1
Q

Decerebration resembles…

A

Supratentorial lesions; central/transtentorial herniation

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2
Q

What is decerebrate rigidity (extensor posturing)?

A

Unopposed hyperactivity in extensor muscles in all limbs. Lesion caudal to red nucleus.

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3
Q

A noxious stimulus administered to a decerebrate patient may ______ the rigidity, or _______ when it is not apparent.

A

Exacerbate; evoke decerebrate posturing

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4
Q

What is the diencephalic stage of central/transtentorial herniation?

A

Before herniation through the tentorial notch

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5
Q

What are symptoms of the diencephalic stage of central herniation?

A
  • decreased level of consciousness
  • lethargy
  • small but poorly reactive pupils
  • eye movement disorders
  • withdrawal reflex to noxious stimuli is intact
  • reflexes are hyperactive
  • bilateral Babinski response
  • may become decorticate (ipsilateral, then contralateral)
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6
Q

After complete central herniation…

A

Patient becomes decerebrate, rapid decline, pupils dilated and fixed, comatose, no eye movement, Cheyne-Stokes respiration, tachypnea, maybe death

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7
Q

Why are flexor muscles inactive in the decerebrate condition?

A

Loss of descending corticospinal and rubrospinal input to flexor motor neurons

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8
Q

Why are extensor muscles unaffected by loss of cortical fibers?

A

Activated by descending reticulospinal and vestibulospinal inputs

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9
Q

Decerebrate rigidity is also known as _______. Why?

A

Gamma rigidity. Descending reticulospinal influence on extensor motor neurons is focused primarily on gamma rather than on alpha extensor motor neurons.

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10
Q

What is decerebellate rigidity?

A

Enhanced activity of vestibulospinal system; extensor hypertonus enhanced compared with that seen with decerebration alone.

(lesion of anterior lobe of cerebellum - cut off inhibitory Purkinje cells)

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11
Q

Why is decerebellate extensor rigidity referred to as alpha rigidity?

A

Increased excitatory activity in vestibulospinal system produces enhanced direct input to alpha motor neurons.

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12
Q

What is decorticate posturing/rigidity?

A
  • flexion of the upper extremities (intact rubrospinal fibers) at the elbow
  • extensor hypertonus in the lower extremities (intact reticu- lospinal fibers)
  • altered state of consciousness and respiration
  • oculomotor deficits
  • range of motor responses from weakness to motionlessness
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13
Q

Lesions of the hemisphere (tumor/hemorrhage) frequently lead to…

A

Decorticate rigidity (removal of cortical influence on brainstem motor nuclei)

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14
Q

What does it mean if a patient passes from decorticate to decerebrate posturing?

A

The lesion is spreading downwards and they are in danger. It is now affecting more caudal brainstem and the patient may eventual lose respiration.

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15
Q

What are nerve conduction studies?

A

Divide distance between stimulating and recording electrodes by the time of travel for action potential; amplitude of the response indicates the number of axons that fired, and shape of the response graph depicts synchrony.

Diseased nerve will not have a sharp wave appearance due to demyelination.

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16
Q

What is a compound muscle action potential (CMAP)?

A

Recording electrode placed over muscle innervated by the stimulated nerve to test: motor axon, neuromuscular junction, muscle fibers

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17
Q

What is electromyography?

A

Recording electrode placed in the muscle and recording made of the depolarization of the muscle fibers following voluntary contraction under three conditions:

1) muscle at rest
2) patient exerting minimal effort,
3) patient exerting maximal effort

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18
Q

What is fibrillation?

A

Myofibers that become denervated have a membrane that is less stable and can fire spontaneously producing fibrillations; these are NOT VISIBLE

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19
Q

What is fasciculation?

A

Spontaneous firing of a motor unit which ARE VISIBLE, cased by unregulated activity of a motor neuron; can be benign or pathological

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20
Q

Reinnervation causes a switch in the characteristics of the myofiber to __________.

A

the new characteristics of the motor neuron which innervated it. Often seen in ALS.

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21
Q

What is myasthenia gravis (MG)?

A

Disease of neuromuscular junction where antibodies bind to nicotinic acetylcholine receptors –> lysis of postsynaptic receptors

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22
Q

What are symptoms of myasthenia gravis?

A
  • weakness waxing/waning
  • ocular muscles most often affected first (65%)
  • 85% cases have limb musculature weakness
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23
Q

What is ocular myasthenia?

What is myasthenic crisis?

A

Confined to ocular muscles.

Weakness involving the respiratory muscles.

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24
Q

How do you treat myasthenia gravis?

A

Acetylcholinesterase inhibitors

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25
Q

What is the stretch reflex?

A

Monosynaptic excitatory connection of Type Ia spindle with alpha motor neuron innervating afferent origin

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26
Q

What is reciprocal inhibition?

A

Type Ia fiber –> Ia interneuron –> Inhibit motor neuron of ANTAGONIST muscle

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27
Q

What is the crossed extensor reflex?

A

Muscle afferents –> interneuron –> CONTRALATERAL side & propriospinal neurons (example: help stand when lifting the other foot)

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28
Q

What are long loop reflexes?

A

Muscle sensory information via ascending pathways to thalamic relay –> cortex –> alter gain on spinal reflexes via descending supraspinal pathways

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29
Q

What is poliomyelitis?

A

Viral disease causing damage to somatic motor neurons in the spinal cord or brainstem; leads to weakness/paralysis

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30
Q

Lesion to decussating corticospinal fibers:

Upper extremity decussates more ______ and lower extremity decussates more ______.

A

rostrally; caudally

Important for localization of lesion.

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31
Q

What is superior alternating hemiplegia (Weber Syndrome)?

A

Hemorrhage in paramedian branches of P1

(1) contralateral hemiparesis (spasticity)
(2) lesion of ipsilateral CNIII - deviation of ipsilalteral eye down and out; direct and consensual light reflex/accommodation LOST ipsilaterally

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32
Q

What is middle alternating hemiplegia (Foville Syndrome)?

A

Occlusion of paramedian branches of basilar a.

1) alternating hemiplegia
(2) ipsilateral CN VI sign
(if ischemia is bad enough can cause loss of DC-ML sense

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33
Q

What is inferior alternating hemiplegia (Dejerine Syndrome)?

A

Occulsion of anterior spinal a.

(1) contralateral hemiparesis of extremities
(2) ipsilateral deviation of tongue on protrusion (CN XII)
(and contralateral fine touch/vibration from DC-ML)

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34
Q

What is multiple sclerosis (MS)?

A

Chronic, degenerative inflammatory disorder, associated with autoimmune disease
- demyelination/degeneration in SC, brainstem, optic nerve weakness, numbness, pain, vision loss

Early symptoms: blurred vision, blind spots, muscle weakness

Typically progresses steadily or can cause acute attacks followed by remission; NORMAL lifespan

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35
Q

What is amyotropic lateral sclerosis (ALS)?

A

Loss of anterior horn motor neurons (lower motor neuron syndrome), potential for loss of cranial motor nuclei and Betz cells.

Typically middle age, extremity weakness, bulbar signs/symptoms, NO SENSORY PROBLEMS (typically), dysphagia, 2-6 yr course post-diagnosis… fatal :(

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36
Q

In ALS:

Astrocytosis is caused by…

A

Loss of lower motor neurons.

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37
Q

In ALS:

Gliosis is caused by…

A

Lateral column degradation (loss of upper motor neurons); “sclerosis” of lateral columns

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38
Q

What is spinal shock?

A

Periods of time following a spinal cord injury, typically a complete spinal cord transection, where there is hyporeflexia/areflexia below the level of the lesion as well as hypotonia.

Reflexes then return over a period of months but are hyperreflexic in nature due to upregulation of postsynaptic neurotransmitter receptors.

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39
Q

What is central cord syndrome (CCS)?

A

Incomplete spinal cord injury, often cervical/upper thoracic from neck hyperextension.

3 big symptoms:

  • lead to weakness of arms and variable sensory loss = inverse paraplegia (arms/hands affected and legs are not)
  • urinary retention
  • patchy loss of ALS sensation below lesion
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40
Q

What are causes of central cord syndrome?

A

Trauma, hemorrhage, ischemia, necrosis of central cord

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41
Q

What are lateral corticospinal fibers not affected in CCS?

A

Lesion is too peripheral

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42
Q

What is anterior cord syndrome?

A

Ischemia to the anterior spinal artery perfused SC region –> loss of motor function below lesion, loss of sensation via ALS but DC not affected

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43
Q

What is posterior cord syndrome?

A

Rare incomplete lesion due to ischemia in posterior spinal artery –> damage to DC causing loss of associated sensation below the level of the lesion

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44
Q

What is tabes dorsalis?

A

Tertiary syphilis in which the DC neurons are demyelinating; more common in males.

Symptoms:

  • weakness,
  • hyporeflexia
  • ataxic gait
  • progressive degeneration of joints
  • sensory ataxia (lack of proprioceptive input)
  • episodes of intense pain and disturbed sensation
  • personality changes
  • dementia
  • deafness
  • visual impairment
  • impaired light response
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45
Q

What is Romberg’s test?

A

Try to maintain balance when eyes are closed. Can help diagnose tabes dorsalis.

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46
Q

Lesion to cervical enlargement:

Damage only to lateral funiculus

A

ipsilateral upper and lower extremity upper motor neuron signs

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47
Q

Lesion to cervical enlargement:

C6-8 anterior horn, lateral funiculus

A
  • lower motor signs in upper extremity ipsilaterally

- upper motor signs in lower extremity ipsilaterally

48
Q

Lesion to cervical enlargement:

anterior horn or alpha motor neurons

A

lower motor signs

49
Q

Lumbosacral injury causes:

A

Damage to anterior horn and corticospinal fibers

Lower motor neuron signs in lower extremity ipsilaterally

50
Q

What is Brown-Sequard Syndrome?

A

Hemisection of spinal cord

  • Ipsilateral loss of motor function (spastic paralysis), proprioception, vibration, fine touch (DC)
  • Contralateral loss of pain, temp, crude touch (ALS) two levels down
51
Q

What is lower motor neuron syndrome?

A

Alpha motor neuron damage

Flaccid paralysis/weakness of corresponding muscle, areflexia, atonia, disuse atrophy, fibrillation or fasciculation (involuntary contraction of one motor unit or a group of motor units)

52
Q

What is upper motor neuron syndrome?

A

(1) Initially flaccid paralysis progressing to spastic
(2) hypertonia
(3) hyperreflexia; typically affect groups of muscles Babinski sign (dorsiflexion)

53
Q

Increased spasticity causes:

A

increased resistance to passive movement (velocity dependent, more resistance for higher vel.)

MOST pronounced in antigravity muscles (proximal flexors in UE and extensors in LE)

54
Q

What is the clasp-knife effect?

A

after relatively brief period of applied force, increased resistance collapses

55
Q

Motor cortex ischemia of primary motor cortex leads to…

A

spastic paralysis, hyperreflexia, etc. (UMN lesion)

56
Q

Motor cortex ischemia of supplementary or pre- motor cortex leads to…

A

apraxia (difficulty using body part to perform voluntary action)

57
Q

An infarction of the posterior limb of the internal capsule can be caused by damage to the ________. This causes:

A

lenticulostriate aa. of MCA

  • contralateral upper and lower extremities affected via weakness, transient flaccid paralysis transitioning to spastic paralysis and other UMN signs
  • Affects axons to neostriatum, thalamus, brainstem, thalamocortical projections (hemisensory loss or homonymous hemianopia can accompany motor loss)
58
Q

What are negative signs of a lateral corticospinal lesion?

A

Loss of independent movements of isolated muscles (digits), hemiparesis, hyporeflexia of superficial reflexes (abdominal reflex)

59
Q

What are positive signs of a lateral corticospinal lesion?

A

Babinski sign – extensor plantar response (upward) and hyperreflexia of tendon reflexes

60
Q

What is hemineglect?

A

Lesion to RIGHT posterior parietal cortex –> inability to make directed limb movements in certain contexts and neglect information from contralateral hemi-field

61
Q

Unilateral damage to corticonuclear fibers of the trigeminal motor nucleus…

A

Does not cause weakness of masticatory mm. (bilateral)

62
Q

What is a central seven lesion?

A

Lesion rostral to facial motor nucleus –> drooping of muscles on lower portion of face opposite the lesion

63
Q

What is Bell’s palsy?

A

Lesion of the root of CN VII –> flaccid paralysis of upper and lower face ipsilaterally

64
Q

A nucleus ambiguus lesion causes…

A

Weakness of palatal arch on side of nucleus (opposite the corticonuclear projection)

Deviation of the uvula opposite the side of LMN lesion and ipsilateral to the UMN lesion (deviation to strong side; side of lesion)

65
Q

A hypoglossal lesion causes…

A

Tongue deviation toward side of LMN lesion and contralateral to side of UMN lesion due to unopposed pull of intact muscle (consider UMN if other corticonuclear lesion signs present)

66
Q

A corticonuclear CN XI lesion causes…

A

SCM and trapezius muscle affected ipsilaterally to internal capsule lesion (in the genu)

Patient is unable to shrug or elevate shoulder affected.

67
Q

What is paraneoplastic syndrome?

A

Antibodies developed against a tumor that attack the brain can cause ataxia due to cerebellar insult

Yo antibody (breast/ovarian neoplasm derived) –> severe ataxia, dysarthria, oculomotor nystagmus

68
Q

A right-sided lesion to the genu and posterior limb of IC causes…

A
  • left spastic hemiparesis (extremities)
  • left central facial paralysis
  • deviation of uvula to right on phonation
  • deviation of tongue to left on protrusion
  • ipsilateral SCM and trapezius mm. paralyzed (variable)
69
Q

What is Kernohan Notch Phenomenon?

A

Herniating uncus displaces midbrain against edge of tentorium cerebelli contralateral to herniation

CN III palsy, and hemiplegia of extremities IPSILATERAL to herniation (FALSE LOCALIZING SIGN)

70
Q

Vestibulocerebellar lesions cause…

flocconodular lobe or midline structures

A

Truncal ataxia, tendency to fall to that side (or forward/backward), wide-based stance, can’t walk heel-to-toe (walk in tandem), nystagmus, tilting of the head

Midline specifically (nodulus, fastigial nucleus): 
- titubation (tremor of axial body or head)
71
Q

What are medulloblastomas?

A

Tumors that commonly arise at the roof of the 4th ventricle and impinge upon the flocculonodular lobe of the cerebellum
- associated cerebellar impairment (ataxia, staggering gait (“drunken sailors gait”), truncal ataxia, nystagmus, issues making smooth pursuit eye movements)

72
Q

What is anterior lobe syndrome?

A

Cerebellar lesion commonly caused by alcoholism leading to degeneration of cerebellar cortex; legs primarily affected, broad-based staggering gait

73
Q

Damage to nucleus interpositus causes:

A
  • dysmetria (issues reaching in space)
  • intention tremor
  • lack of coordinated joint motions (Pendular reflex)
74
Q

Why are visceral deficits related to cerebellar lesions are rarely reported?

A
  • Somatomotor deficits are overwhelmingly diagnostic and there is no need to look further
  • Cerebellar lesions may cause increase in intracranial pressure and pressure on the medulla; can be hard to separate from deficits caused by pressure on the medulla
75
Q

Lesion to lateral hemispheres of cerebellum (neocerebellar syndrome) can cause… (I’m really sorry)

A
  • dyssenergia
  • ataxia of extremities
  • dysmetria
  • intention tremor
  • delayed initiation of movement
  • static tremor
  • dysdiadochokinesia
  • dysarthria
  • rebound phenomenon
  • oculomotor dysfunction (nystagmus)
  • hypotonia
76
Q

What is dyssenergia?

A

Decomposition of movement (complex movements requiring multiple muscles are performed with one muscle at a time)

77
Q

What is dysmetria?

A

inability to stop movement at appropriate time or direction (past-pointing) – hypermetria and hypometria

78
Q

What is dysdiadochokinesia?

A

irregular pattern of movement when patient performs rapid, alternating movements – palms up/down

79
Q

What is dysarthria?

A

disorder of speech where mechanical aspect of articulation is impaired; slurred/garbled speech

Scanning speech: alternating slow or staccato speech in nature

80
Q

What is rebound phenomenon?

A

impaired check; inability of agonist and antagonist muscles to adapt to rapid changes in load

81
Q

What is intention/kinetic tremor?

A

Unregulated contraction and relaxation of agonist and antagonist muscles during movement)

For example, little/no tremor at rest, but finger tremor markedly increases as it approaches nose

82
Q

What is a static tremor?

A

Manifested when patient stands with arms extended; Rhythmic movement of shoulders and also upper extremities

83
Q

Vestibular nystagmus often presents when gaze is directed ______ and the fast component is directed ________.

A

contralaterally; away from side of lesion

84
Q

Symptoms of basal ganglia motor disease include:

A
  • Chorea
  • Hemiballismus
  • Athetosis
  • Tardive dyskinesia
  • Huntington’s disease (Hyperkinesia)
  • Parkinson’s disease (Hypokinesia)
  • Sydenham’s Chorea
  • Babinski sign
  • Clonus
  • Hyperreflexia
  • Spasticity (clasp knife)
  • Spastic Gait
85
Q

What is believed to be a cause of schizophrenia?

A

Increased number and sensitivity of the D2 (dopamine) receptors within striatal neurons such that treatment often involves blocking (or down-regulating) the D2 receptors.

86
Q

What is clonus?

A

Loss of UMN –> absence of inhibition of antagonists muscles –> repetitive sequential contraction of limb flexors and extensors, typically seen with spasticity and hyperreflexia

87
Q

What is fetal alcohol syndrome?

A

Alcohol toxic to brain, specific susceptibility is present for brain regions preferentially affecting LARGE POSTMITOTIC neurons, PERMANENT defects

  • craniofacial dysmorphia (short palpebral fissures, flat midface, abnormal premaxillary zone)
  • retardation (growth and neural); MAJOR loss of vermal Purkinje cells and dendritic area
  • enlarged ventricles
  • agenesis of corpus callosum and anterior commissure
  • neural tube defects
  • abnormal neuron/glial proliferation and migration
  • altered hippocampal circuitry
88
Q

What is a hyperkinetic dyskinesia?

A

abnormal involuntary movements; typically from disruption of indirect pathway –> imbalance between excitation and inhibition –> more activity via the cerebral cortex

89
Q

What are choreiform movements?

A

generalized random dance-like movement patterns; commonly with damage to indirect pathway (Huntington’s)

90
Q

St. Vitus’ Dance is a type of choreiform movement; describe it.

A

normal progression of movements cannot occur such that a person can only perform one movement pattern for a few seconds then rapidly switch; this occurs from diffuse damage to caudate and putamen (inhibitory GABA-ergic neurons)
- May have a decrease in muscle tone

91
Q

What is athetosis?

A

Slow writhing movements of distal extremity or face; when brisk are referred to as choreoathetosis; when resembling dystonia called athetotic dystonia

92
Q

What is hemiballismus?

A

Uncontrollable succession of violent/flailing movements every few seconds – once every few minutes, location and extent of movement varies (usually upper extremity)

Results from subthalamic nucleus lesion –> no interaction from subthalamic nucleus to globus pallidus which is essential for smooth/progressive/rhythmic movements

93
Q

What is akinesia/hypokinesia?

A
  • Impaired ability to initiate movements due to deficiency in ability to plan or guide movement to desired position
  • Generalized disruption of basal nuclei for planning and generating programmed movements
94
Q

What is bradykinesia?

A

Reduced velocity and amplitude of movement due to disruption of balance between outflow of direct and indirect pathways to thalamus
- increase in activation of the antagonist muscles and inappropriateness causes movement impairment (not necessarily due to overall decrease in muscle activity)

95
Q

What are hypokinetic disorders?

A

can be considered lesions of the neostriatum (between that and internal globus pallidus). Direct pathway!

  • Parkinson’s
  • Huntington’s
  • Wilson’s
  • Tardive dyskinesia
96
Q

What is Parkinson’s disease?

A

Loss of melanin-containing dopaminergic neurons in the nigral complex has the net effect of decreasing thalamocortical neuronal activity. Most common disease of basal ganglia.

97
Q

Parkinson’s progression:

A
  • First sign (asymmetric gait, vague clumsiness, less blinking, reduced arm swinging)
  • progressive onset of movement and affective disturbances (pill-rolling tremor, cogwheel rigidity, akinesia, bradykinesia, disturbances of eye movement, loss of postural reflexes)
  • progressive decline in cognitive function (bradyphrenia, dementia, memory dysfunction)

Order of affection: motor to executive to motivational/visuomotor; lateral to medial within substantia nigra

98
Q

Symptoms of Parkinson’s:

A

Rhythmical tremor, lead-pipe rigidity, bradykinesia and hypo/akinesia, stooped posture with shuffling gait (Simian posture), dementia, Myerson’s sign

99
Q

What is rhythmical tremor?

A

Occurs during rest, NOT during voluntary activity,
- involving jaw, lips, lower facial muscles, limb(s) – begins unilaterally, likely from oscillating states of activity for extensor and flexor control resulting from lack of subthalamic nucleus input

100
Q

What is lead-pipe rigidity?

A

“cogwheel rigidity” such that when moved the rigid limb remains where placed and when externally moved the limb periodically gives way and then resistance is reestablished

101
Q

What is Myerson’s sign?

A

repetitively tapping forehead produced uncontrollable blinking

102
Q

How is Parkinson’s treated?

A
  • L-DOPA and carbidopa (3-5 years)
  • Dopamine agonists
  • Deep brain stimulation (subthalamic nucleus); treat the tremor
  • Pallidotomy / Thalamotomy (last resort)
103
Q

Risk factors for Parkinson’s?

A
  • Familial (mutation in alpha-synuclein)
  • Environmental risk through exposure to trichloroethylene, perchloroethylene, and carbon tetrachloride
  • Trauma (boxers)
104
Q

Histological findings in Parkinson’s:

A
  • Loss of dopaminergic neurons in SNc (lateral to medial) degradation of nigrostriatal fibers so NO dopamine in neostriatum
  • Cytoplasmic Lewy bodies and alpha-synuclein
  • Overall decrease in thalamic facilitation signals = bradykinesia/hypokinesia (first affects motor loop then executive loop)
105
Q

What is the progression of Huntington’s disease (onset age 35-44)?

A
  • Psychiatric problems (abnormal behavior), likely the projections from frontal cortex to caudate; caudate nucleus forms a concave depression in the normal region (caudate nucleus affected first, but entire basal ganglia affected)
  • Dementia
  • Chorea
  • Hyperkinetic state
  • Terminal stage (rigidity, dystonia, death as akinetic mute in 15 years post-onset)

Progression is dorsal to ventral, medial to lateral, anterior to posterior; executive loop, motor loop, motivational last

106
Q

Glutamate excitotoxicity is thought to be mainly responsible for diminution of glucose metabolism early in Huntington’s. How does this work?

A

Unknown mechanism causes glutamate to persist at one type of receptor, the N-methyl-D-aspartate (NMDA) receptor, which opens calcium ion channels. The resulting excessive influx of calcium causes an increase in intracellular calcium, which triggers a cascade that leads to cell death.

107
Q

The basal ganglia’s involvement in the limbic loop can lead to ______ in Huntington’s and Parkinson’s patients.

A

dementia

108
Q

What is Sydenham’s chorea?

A

Involuntary movements involving the face, tongue and limbs seen in childhood (girls more than boys) following streptococcal infection (GAS) or acute rheumatic fever

  • Other SX: irritability, emotional lability, obsessive-compulsive behaviors, attention deficit, anxiety
109
Q

What causes Sydenham’s chorea?

A

Caused by auto-antibodies arising from similar epitopes (between neural tissue and viral antigens) – lasts 3-6 weeks
- Some issues with recurrence over next several months or years is seen

110
Q

What is Wilson Disease?

A

Hepatolenticular degeneration related to basal ganglia damage (autosomal recessive)

  • onset between 11-25yr
  • disorder of copper metabolism –> accumulation within the liver, cirrhotic nodules and progressive liver damage and damage to brain regions (lenticular nucleus)
  • Liver damage signs precede detection of brain damage
111
Q

List symptoms of Wilson Disease

A
  • psychiatric symptoms (personality)
  • tremor
  • dysarthria
  • diminished dexterity
  • unsteady gait
  • rigidity
  • mask-like facial expression, gaping mouth
  • Kayser-Fleischer rings
112
Q

What are Kayser-Fleischer rings?

A

Aminoaciduria from excessive amounts of amino acids in urine –> copper accumulation within the cornea

113
Q

What changes are seen in the brain due to Wilson Disease?

A 
Degeneration of 
- putamen (small cavities)
- thalamus
- head of caudate
- frontal/cerebellar cortices 
(from loss of neurons, axon degeneration, increasing protoplasmic astrocytes)
114
Q

Treatment of Wilson Disease?

A

Decrease amount of copper within the body via chelating agents (TETA) and penicillamine –> decrease in signs 5-6mo from onset of treatment

115
Q

What is tardive dyskinesia?

A

Basal nuclear disorder caused by medical intervention for another disease

Uncontrolled involuntary movements, (face, mouth, tongue) cogwheel rigidity – these are temporary or permanent

116
Q

What medical interventions cause tardive dyskinesia?

A

Chronic treatment with neuroleptic medications (chloropromazine, haloperidol) which BLOCK dopaminergic transmission throughout the brain (D2 receptors)
–> imbalance in nigrostriatal influence (dopamine SUPERSENSITIVITY) in basal motor loop (movement disorders)

117
Q

Treatment of tardive dyskinesia?

A

Withdrawal of causative medication –> EXACERBATION of psychotic state

Neuroscience BB Exam 3 (9 decks)

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