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Pod Med III > 6) Neurologically Mediated Disorders of Muscle Control > Flashcards

6) Neurologically Mediated Disorders of Muscle Control Flashcards

1
Q

Cerebellum main function

A
  • Motor control
  • Enables smooth, well timed, proportional responses
  • Speech, emotions, as well as pleasure and fear
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2
Q

Cerebellum controls

A
  • Unconscious posture and balance

- Coordination of smooth voluntary movement

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3
Q

Lobes of the cerebellum

A
  • Paleocerebellar (anterior)
  • Flocculonodular (middle)
  • Neocerebellar (posterior)
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4
Q

Paleocerebellar (anterior) lobe function

A
  • Unconscious posture, balance and proprioception
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5
Q

Flocculonodular (middle) lobe (aka vestibulocerebellum) function

A
  • Vestibular – unconscious equilibrium
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6
Q

Neocerebellar (posterior) lobe function

A
  • Receives input from cerebral motor cortex

- Coordinates voluntary skilled movements

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7
Q

Cerebellum afferent input

A
  • Cerebral cortex
  • Vestibular tracts
  • Spinocerebellar tract
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8
Q

Cerebellum efferent input

A
  • Integrates afferent “input” plus data from red nucleus and basal ganglia
  • Relayed to cerebral motor cortex voluntary initiation of movement
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9
Q

Somatotopic arrangement in vermis

A
  • The unpaired, median portion of the cerebellum

- Connects the two hemispheres

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10
Q

Dyssynergia

A
  • Decomposition of movement
  • Inability to perform voluntary movements smoothly
  • Lack of normal coordination between agonists, and synergists
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11
Q

Dyssynergia recognition

A
  • Use of accessory muscles
  • Wide arc of motion
  • Asthenia
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12
Q

Asthenia

A
  • Weakness
  • Lack of energy and strength
  • Hyporeflexia
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13
Q

Dysrhythmia

A
  • Abnormal timing and coupling of movement
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14
Q

Dysmetria

A
  • Inability to gauge distance, speed, strength and velocity
  • Excessive rebound
  • Delay in initiation or cessation of movement
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15
Q

Intention tremor

A
  • Exacerbated at end of goal-related movement

- Medium frequency tremor

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16
Q

Staccato speech

A
  • Slurred, jerky or explosive
  • Syllabic
  • Clipped like speech
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17
Q

Nystagmus

A
  • Rapid jerky eye movements
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18
Q

Signs of cerebellar damage

A
  • Dysdiadokinesia / Dysmetria
  • Ataxia
  • Nystagmus
  • Intention tremor
  • Speech (slurred or scanning)
  • Hypotonia
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19
Q

Ataxic gait

A
  • Wide based gait
  • Slow, jerky cadence
  • Stride length and foot placement vary with each step
  • Frequent loss of balance
  • Patient performs numerous “adjustments”
  • Two-phase foot contact (heel then toe “double tap”)
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20
Q

Cerebellum ataxic gait treatment

A
  • Palliative (primary)
  • Increase stability during ambulation
  • Quad cane
  • Walker
  • Physical therapy
  • Functional or accommodative orthoses
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21
Q

Cerebellum clinical evaluation

A
  • Carries unconscious proprioception
  • Romberg’s Test
  • Coordinates smooth volitional movements
  • Heel to shin test
  • Alternate patting test
  • Gait analysis ataxic
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22
Q

Ataxic gait clinical evaluation

A
  • Paleocerebellar lesion
  • Disturbance of equilibrium
  • Neocerebellar hemispheres
  • Classic signs of ataxic gait
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23
Q

Basal ganglia

A
  • Control intentional movement
  • Responsible primarily for motor control
  • Collection of nuclei deep within brain
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24
Q

Basal ganglia nuclei

A
  • Receive input from pre-motor cortex regarding “planned movement”
  • Efferent pathways then control movement
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25
Q

Basal ganglia involved with movement

A
  • Caudate
  • Putamen
  • Substantia nigra
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26
Q

Basal ganglia lesions result in

A
  • Awkward unintentional movements
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27
Q

Striatum (caudate and putamen)

A
  • Primarily inhibitory effect on thalamus
  • Receive input from cerebral cortex
  • Relay this input to globus pallidus
  • Globus pallidus outputs to thalamus
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28
Q

Striatum (caudate and putamen) neurotransmitters

A
  • Acetylcholine

- γ-Aminobutyric acid (GABA)

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29
Q

Striatum (caudate and putamen) injury results in

A
  • Hyperkinetic disorders

of movement

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30
Q

Substantia nigra

A
  • Communicates directly with striatum
  • Deterioration results in hypokinetic disorders
  • Neurotransmitter is dopamine
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31
Q

Substantia nigra primary function

A
  • Eliminates excessive movement
  • Keeps the body still when it needs to be still
  • Allows the body to move without extraneous movements
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32
Q

Huntington’s chorea

A
  • Chronic progressive degenerative CNS disorder

- Selective loss of caudate and putamen

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33
Q

Huntington’s chorea incidence

A
  • Autosomal dominant transmission
  • Defect in chromosome 4
  • Occurs in all ethnic and racial groups
  • 5 to 10/100,000
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34
Q

Huntington’s chorea characteristics

A
  • Choreic (dance-like) involuntary movement
  • Progressive dementia
  • Psychiatric and behavioral disturbances
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35
Q

Huntington’s chorea shows extensive hypertrophy of

A
  • Basal ganglia
  • Cerebral cortex
  • Cerebellum
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36
Q

Huntington’s chorea treatment

A
  • No drug to attenuate the disease process
  • Can only minimize symptoms
  • Tetrabenazine (Xenazine)
  • Deutetrabenazine (Austedo)
  • Haloperidol
  • Phenothiazines
  • Antidepressants
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37
Q

Sydenham’s chorea

A
  • Sequella of Group A β-hemolytic strep infection
  • Major diagnostic criteria for rheumatic fever
  • Most important form of childhood chorea
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38
Q

Sydenham’s chorea characteristics and incidence

A
  • Autoantibodies target basal ganglia cells
  • Peak incidence – 8 years old
  • More common in females
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39
Q

Syndeham’s chorea clinical recognition

A
  • Insidious onset
  • Emotional lability
  • Facial grimacing
  • Involuntary flinging movements
  • Exacerbated with attempts to control movements and abate while sleeping
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40
Q

Sydenham’s chorea diagnosis

A
  • ASO titres
  • ↑ acute phase reactants
  • Acute-phase reactants, the erythrocyte sedimentation rate (ESR), and C-reactive protein levels (CRP) are usually elevated at the onset of Acute Rheumatic Fever
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41
Q

Huntington’s disease vs. Sydenham’s chorea

A
  • Huntington’s = progressive, and ultimately, fatal disease

- Sydenham’s chorea = treatable and curable

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42
Q

Sydenham’s chorea treatment

A
  • Penicillin or erythromycin

- Must be continued for minimum of 10 days

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43
Q

Palliative treatment of Sydenham’s chorea

A
  • Valproic acid
  • Carbamazepine or haloperidol
  • Minimize external stimuli
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44
Q

Parkinsonism is characterized by

A
  • Tremor
  • Muscular rigidity
  • Bradykinesia
  • Alterations of posture and attitude of extremities
  • Paralysis agitans
  • Festination
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45
Q

Parkinsonism etiologies

A
  • Exposure to environmental toxins
  • Free radical generation
  • Inheritance (?)
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46
Q

Parkinsonism prevalence

A
  • 1% of population

- 50,000 new cases per year

47
Q

Parkinsonism disease progression

A
  • Slow and gradual

- With treatment – normal life expectancy

48
Q

Parkinsonism pathology

A
  • Loss of dopaminergic neurons in substantia nigra

- 80% of neurons are lost before disease is evident

49
Q

Parkinsonism clinical features

A
  • Tremor (pill rolling)
  • Rigidity
  • Bradykinesia (slow movement)
  • Gait and posture disturbances
50
Q

Resting tremor (parkinsonism)

A
  • “Pill rolling” – 4 – 6 Hz
  • Initial complaint ~75% of time
  • Begins one-sided – usually a hand
51
Q

Cog-wheeling (Parkinsonism)

A
  • A jerky feeling in your arm or leg
52
Q

Rigidity (Parkinsonism)

A
  • Stooped posture

- Shuffling gait

53
Q

Bradykinesia (Parkinsonism)

A
  • Slowness with muscular fatigue – “freezing”

- Akinesia or lack or “poverty of motion”

54
Q

Loss of facial expression (Parkinsonism)

A
  • Monotonous, stuttering, “deliberate” speech

- Masked facies due to muscular fatigue

55
Q

Parkinsonism gait disturbances

A
  • Shuffling gait
  • Development of a forward or backward lean
  • Festination
  • Retropulsion
56
Q

Festination

A
  • Correction of forward lean
  • Sudden short shuffling steps
  • Become progressively shorter and faster
57
Q

Retropulsion

A
  • Correction of backward lean

- Rapid backwards steps

58
Q

Parkinsonism pharmacologic intervention

A
  • Replace dopamine (levodopa, carvidopa)
  • Dopamine agonists (peroglide)
  • Selegine (MAO inhibitor, delays need for levodopa)
  • Amantadine
  • Anticholindergics
  • COMT inhibitors
59
Q

Parkinsonism surgical intervention

A
  • Globus pallidus pallidotomy (relieves dyskinesias)
  • Deep brain stimulation (relieves tremors and dyskinesias, electrode placed within thalamus)
  • Fetal nigral transplantation (implantation of fetal cells, experimental)
60
Q

Wilson’s disease

A
  • Accumulation of copper in tissue
  • Defect in ceruloplasmin (carries copper around your body to the tissues that need it)
  • Autosomal recessive inheritance
61
Q

Wilson’s disease symptoms

A
  • Basal ganglia disorders
  • Hepatic cirrhosis
  • Kayser-Fleischer Rings (RINGS AROUND THE IRIS)
  • Arm flapping
62
Q

Wilson’s disease treatment

A
  • C-penicillamine
63
Q

Essential tremor

A
  • Generally postural

- Autosomal inheritance with incomplete penetrance

64
Q

Essential tremor incidence

A
  • Late adolescence
  • Older adulthood
  • Male to female – 1:1
65
Q

Essential tremor clinical recognition

A
  • Typically occurs when hands are in use
  • Average tremor 6 – 8 Hz
  • Physiologic and emotional stress exacerbate symptoms
66
Q

Essential tremor treatment

A
  • Symptoms relieved with alcohol
  • Propranolol
  • Anti-seizure medication
  • Tranquilizers
  • Botox injections
67
Q

Cerebral palsy

A
  • Chronic, non-progressive motor dysfunction

- Evident within first two years of life

68
Q

Cerebral palsy incidence

A
  • 1.5 - 7.5 per 1000 live births

- Greater incidence in low birth weight infants

69
Q

Cerebral palsy (prenatal)

A
  • Often idiopathic
  • Genetic disease
  • Maternal disorders (gestational diabetes, Rh incompatibility, toxemia)
  • Fetal malformations
  • Presence of more than one fetus (crowding)
70
Q

Cerebral palsy (natal)

A
  • Most common etiology
  • Any process or insult at the time of delivery or within the first week
  • The majority of CP (85%–90%) is congenital
71
Q

Natal cerebral palsy common etiologies

A
  • Prematurity
  • Anoxia
  • Respiratory distress
72
Q

Postnatal cerebral palsy

A
  • Injury from one week to two years of age
73
Q

Kernicterus

A
  • Atype of brain damagethat can result from high levels of bilirubin in a baby’s blood
  • It can cause athetoid cerebral palsy and hearing loss.
74
Q

Postnatal cerebral palsy frequent etiologies

A
  • Anoxia
  • Encephalitis
  • Infection
  • Poisoning
  • Seizures
  • Trauma
  • Intracranial Hemorrhage
  • Periventricular Leukomalacia
75
Q

Pyramidal cerebral palsy

A
  • Spastic”
  • Most common presentation – 64% of cases
  • Lesion located in periventricular
76
Q

Pyramidal cerebral palsy is characterized by

A
  • Lesion in premotor cortex
  • Upper motor neuron lesion
  • Increased resistance to passive range of motion
  • Delayed motor milestones
  • Retention of primitive reflex responses
  • Lesion location typically periventricular
77
Q

Periventricular leukomalacia

A
  • Affects the corticospinal tract, optic and acoustic radiations
  • Intraventricular hemorrhage
78
Q

Pyramidal CP hemiplegia (30%)

A
  • Two limbs on same side of body
  • Upper extremity more involved
  • Spastic limbs are thinner and smaller
  • Associated with leg length discrepancy
  • Babinski sign present in post natal cases
79
Q

CP Diplegia/paraplegia (20%)

A
  • Paralysis of legs

- Paraplegia may affect arms but to a lesser extent

80
Q

CP quadriplegia (13%)

A
  • Involves all four limbs equally

- Double hemiplegia – arms more severely involved than legs

81
Q

Extrapyramidal CP athetosis (11%)

A
  • Post natal Kernicterus
  • Undergo “athetoid” shift with bracing or surgery
  • Snake like movement
82
Q

Extramyramidal CP hypotonia (5%)

A
  • Motor cortex lesion

- Decreased or absent muscle tone

83
Q

Extrapyramidal CP rigidity (5%)

A
  • Lead pipe or cogwheel rigidity

- Resistant to motion greatest with slow stretch

84
Q

Extrapyramidal CP tremor (1%)

A
  • Rhythmic, alternating movements

- Occur with rest or voluntary movements

85
Q

Extrapyramidal CP ataxia (5-10%)

A
  • Cerebellar dysfunction
  • Balance disturbance
  • Presence of intention tremor
86
Q

Pyramidal tract disease gait abnormalities

A
  • Increased flexor tone
  • Equinovarus foot deformities
  • “Scissored” Gait
87
Q

Scissor gait

A
  • Internally rotated hips with adduction of leg
  • Arms adducted at shoulders and flexed at wrists and knees
  • Toe walking
88
Q

Athetosis

A
  • Slow serpentine movements
  • Extreme postures vary between flexion with supination and extension with pronation
  • Limb postures asymmetric
  • Concomitant rotary movements of neck
89
Q

Equinus

A
  • Spastic Gastrocsoleus
  • Most common deformity
  • Treat with night splints, orthoses
    Surgical intervention
90
Q

Pes varus

A
  • Continuous activity of posterior or anterior tibial muscle
  • Swing phase activity of posterior tibial muscle
  • Decreased peroneal activity
91
Q

Cavus foot

A
  • Calcaneal inclination angle > 25°

- Complication of spastic gastrocsoleus correction

92
Q

Forefoot equinus

A
  • Dynamic muscular imbalance

- Flexor stabilization secondary to spastic gastrocsoleus

93
Q

Metatarsus adductus

A
  • Spasm of adductor hallucis
94
Q

Cerebral palsy treatment

A
  • Physical and occupational therapy
  • Bracing
  • Botox
  • Temporary relief of spasm
  • Prevents exophytic release of acetylcholine
  • Denervates muscle resulting in flaccid paralysis
  • Toxic effects limited to peripheral nervous system!
95
Q

Multiple sclerosis

A
  • Focal or patchy destruction of myelin sheaths of central nervous system
  • Recurrent attacks of focal or multi-focal neurologic dysfunction
96
Q

Multiple sclerosis mechanism

A
  • Autoimmune disease that destroys CNS elements
  • Dysregulated autoreactive T-cells that cross into the CNS
  • Works together with beta cells and macrophages
  • Inflammatory reaction creates additional demyelination and tissue injury
97
Q

Multiple sclerosis degeneration

A
  • Primary cytodegeneration is the initial event
  • Possibly focused on the oligodendrocyte myelin complex
  • Highly antigenic constituents are released
  • This is what causes CNS degeneration
98
Q

MS onset

A
  • Between third and fourth decade

- Females: ~60%

99
Q

MS genetic factors

A
  • Positive family history → 8-fold increased risk
  • Associated with histocompatibility loci
  • Defect of chromosome 6
100
Q

MS regional factors

A
  • Higher latitude

- Risk seems to be inversely proportional to sunlight exposure

101
Q

MS autoimmune factors

A
  • Molecular mimicry
  • Anti-viral response against myelin
  • Super antigenic stimulation of T-cells
102
Q

MS additional factors

A
  • Tobacco
  • Vascular comorbidities
  • Epstein Barr virus??
  • Gut flora???
  • Emotional or physiologic stress
  • There is a correlation between the level of serum vitamin D and MS risk
103
Q

MS classification

A
  • Benign - 10%
  • Relapsing-remitting – 40%
  • Secondary chronic progressive – 40%
  • Primary progressive – 10%
104
Q

MS pathology

A
  • Scattered areas of demyelination (plaques)
  • Deficit from a few mm to several cm
  • Often paraventricular areas of cerebrum, brainstem and spinal cord
  • Affects white matter predominantly
  • Peripheral nervous system is generally spared
105
Q

MS first attack

A
  • Single symptom – 45%
  • Multiple symptoms – 55%
  • Optic neuritis
  • Generally unilateral
  • 40% of patients
106
Q

MS early symptoms

A
  • Numbness
  • Ataxia
  • Muscular weakness
  • Diplopia
107
Q

MS diagnosis

A
  • Two episodes of neurologic deficit
  • Objective clinical signs of lesions at more than one site in the CNS
  • CT or MRI confirming presence of second lesion
108
Q

MS clinical presentation

A
  • Ocular: Impaired vision, nystagmus
  • Cerebellar: Ataxia, intention tremor
  • Sensory: Dorsal column symptoms
  • Motor involvement: Dependent upon location of lesion
109
Q

Myasthenia gravis

A
  • Acquired autoimmune disorder

- Antibodies formed against acetylcholine receptors

110
Q

Myasthenia gravis incidence

A
  • 0.25 to 2 per 100,000
  • Early onset: < 40 years (slightly higher in females, 60% HLA-B8 and DR3, thymus gland involvement)
  • Late onset: > 40 years (slightly higher in males, no thymus gland involvement)
111
Q

Myasthenia gravis clinical features

A
  • Painless muscular fatigue and weakness
  • Ocular: generally bilateral ptosis and diplopia
  • Bulbar and facial weakness: reduced facial expression
  • Limb weakness: more pronounced proximally
  • Dyspnea on exertion
112
Q

Lambert-Eaton Myasthenic Syndrome

A
  • Acquired autoimmune disease

- Number of acetylcholine “quantals” released is affected

113
Q

Lambert-Eaton Myasthenic Syndrome incidence

A
  • Males to females – 1:1

- Often associated with small cell carcinoma of the lung (more than 50%

Pod Med III (8 decks)

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