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Clinical Medicine III > Exam I > Flashcards

Exam I Flashcards

1
Q

Hierarchical processing

A

higher level of CNS are concerned with abstract processing of information and lower levels bring in/send information

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2
Q

Parallel processing

A

the same signal might reach different brain structures simultaneously for processing (divergent), but different purposes.

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3
Q

Spinal cord connections

A

Hierarchically ‘lowest level employees’ – responding to sensory inputs and following ‘orders’ from action systems

Involved in initial signal reception and final execution of voluntary/involuntary movements (final common pathway)

Basic/simple signal processing – spinal reflexes

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4
Q

Brain Stem connections

A

‘Middle management’ - contain important control centers (sensory and motor) for postural control and locomotion, Receives inputs from head/neck, vestibular and visual systems, sends somewhat processed signals to sensory/perceptual centers, contain motor nuclei for descending pathways to neck/face/eyes, and extra pyramidal pathways

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5
Q

Cerebellar connections

A

‘back-channel employee’ needed for comparing and calibrating movements, contains feedback and feedforward mechanisms. it has Indirect influence on motor outputs to generate smooth coordinated movements, important center for coordination and postural control during movements.

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6
Q

Thalamus connections

A

The ‘doorkeeper to the boardroom’

Acts as a junction, a relay center for signal processing

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7
Q

Basal Ganglia connections

A

Involved in higher order motor planning for coordinated movements

Receives inputs from many areas of cerebral cortex

Sends output back to motor cortex via thalamus

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8
Q

Cerebral Cortex connections

A

Highest executive level of motor control hierarchy, Has direct control on voluntary movements by activating/controlling motor neurons via corticospinal/corticobrainstem pathways

Interacts with other high level association cortical areas (premotor/SMA) to form motor plan/strategy

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9
Q

cross-modal processing

A

Information from muscle spindles, joints receptors, cutaneous receptors, etc., are integrated to give accurate information about movements in a limb

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10
Q

Primary motor cortex connections

A

Primary motor cortex have one-to-one connection (somatotopy) to the level of single motor neuron in spinal cord.

However, convergent and divergent parallel pathways are possible– one cortical site can be connect to a bunch of motor neurons (hence muscles) and one muscle can also potentially be connected to many neurons in a cortical site.

Important for recovery after injuries

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11
Q

Supplemental Motor Area

A

controls internally generated movements, also controls learned motor programs, but can transfer those programs to primary motor cortex after extensive training, also involved in planning complex motor programs

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12
Q

Premotor (PM) area

A

controls movements activated by external stimuli, like visual cues, e.g., ‘go’ when signal changes to green

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13
Q

Necrosis

A

severe injury - cellular swelling (osmosis), fragmentation of structure and cell disintegration, inflammatory response

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14
Q

Apoptosis

A

programmed cell death, no inflammatory reaction

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15
Q

Excitotoxicity

A

when neurotransmitters rise above normal levels – opens ion channels leads to excessive entry of Ca2+ ions – triggers all kinds of harmful cellular pathways – cell death

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16
Q

anesthesia

A

If all sensory modalities lost/absent

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17
Q

hypoesthesia

A

if partial loss of somatosensory

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18
Q

hyperesthesia

A

if somatosensory is hypersensitive

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19
Q

Parasthesia

A

unpleasant sensations like burning, tingling, pricking, numbness with/without sensory stimulus

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20
Q

Allodynia

A

painful sensation to a normal stimulus that should not be painful

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21
Q

Hyperalgesia

A

increased painful sensations to normally painful stimulus

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22
Q

Peripheral vestibular disorders

A

Nerve problems - vestibular neuritis (infection of nerve), perilymph fistula, Meniere’s disease

Canal problems - BPPV

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23
Q

Central vestibular disorders

A

Stroke in brainstem/cerebellum
Cerebellar degeneration
Arnold-Chiari malformation (cerebellum is coming out of foramen magnum

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24
Q

Nystagmus from peripheral lesions

A

Direction-fixed beating
Follows Alexander’s and Ewald’s laws
Beating increases as eyes are moved towards the fast phase
Beating occurs in the plane of impaired canals
Able to fixate with gaze stabilization
Habituates/compensates rapidly with time
Good outcomes with vestibular rehab
Examples of disorders – vestibular neuritis, BPPV

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25
Q

Nystagmus from central lesions

A

Pure vertical or pure torsional or direction-changing beating depending on gaze
Does not follow Alexander’s law
Unable to fixate with gaze stabilization
Takes longer to habituate/compensate
Worse (than peripheral) outcomes
Examples of disorders – Stroke in brainstem/cerebellum, medications

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26
Q

Patterns of motor deficits for UMN disorders

A

Paresis/paralysis
Abnormal tone - spasticity
Abnormal reflexes
Loss of fractionated movements/abnormal synergies
No atrophy
Abnormal co-contractions - CP

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27
Q

Patterns of motor deficits for LMN disorders

A

Paresis/paralysis
Decrease in muscle tone - flaccidity
Decrease in reflex activity
Neurogenic atrophy – due to lack of trophic support to muscles

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28
Q

Tone

A

resistance to passive stretch

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29
Q

Hypertonia results from…

A

results from increased baseline muscle sensitivity to stretch through mechanisms like loss of descending inhibitory control on motor neurons, loss of presynaptic inhibition, denervation hypersensitivity, etc.

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30
Q

Hypotonia results from…

A

results from decreased lower motor neuronal (LMN) activity on muscles due, damage to peripheral nerve, or due to other subcortical lesions, in cerebellum, or from developmental delays

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31
Q

Spastic paralysis caused by UMN lesions

A

velocity-dependent hypertonia

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32
Q

Flaccid paralysis can be caused by…

A

LMN lesions (due to decreased neuronal activity on muscles), or immediately after UMN lesions (as a result of shock).

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33
Q

Rigidity

A

caused by extrapyramidal lesions - velocity-independent hypertonia

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34
Q

UMN - Signs of spastic paralysis

A

weakness, increased tone, increased reflexes, spastic patterns/synergies (eg, flexors for UE and extensors for LE in stroke)

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35
Q

LMN - Signs of flaccid paralysis

A

weakness, decreased tone, decreased reflexes, muscle atrophy, fasciculations and fibrillations, eg, polio, peripheral nerve injuries

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36
Q

spastic pattern

A

Abnormal stereotypical patterns of movements that cannot be adapted – muscles are tightly linked, typically associated with stroke

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37
Q

spastic synergies

A

Typical flexion and extension synergies of UE and LE, person perform voluntary movements in these patterns, typically associated with stroke

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38
Q

Movement problems associated with cerebellum

A

delayed timing, dysmetria (errors in force, ROM, direction), dyesynergia (incorrect sequence of muscle activation), dysdiadokokinesia (difficulty with RAM), Intention tremors (involuntary rhythmic oscillations), and rebound phenomenon (inability to terminate movements), all of these make up ataxic gait, more include dysarthria and asthenia

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39
Q

Movement problems associated with basal ganglia

A

hypokinesias, hyperkinesias such as chorea (twitching, jerking movements), athetosis (writhing, twisting movements), Ballismus (violent, flinging movements), resting tremors

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40
Q

Resting tremor

A

When body is supported and relaxed, hallmark of PD

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41
Q

Intention Tremor

A

Target related movements
Hallmark of cerebellar dysfunction

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42
Q

Ataxic gait

A

cerebellar lesions – wide-based staggering gait, excessive trunk movements, arms wide out, lack of arm swing, LOBs towards ipsilateral side, difficulty in maintaining a line.

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43
Q

Parkinsons gait

A

short shuffling gait with festinations, freezing, difficulty turning, tremor in arms at times

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44
Q

Scissoring gait

A

in spastic CP due to adductor spasticity

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45
Q

Hemiplegic gait

A

circumducting or hip hiking due to LE extensor spastic synergies, arm in flexor synergy

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46
Q

Neuropathic gait

A

high steppage gait due to DF weakness and diminished sensation from feet, eg, diabetic neuropathy

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47
Q

Right hemisphere deficits

A

Spatial deficits – hemineglect, tactile extinction (more common with right-side lesions)

Non-spatial deficits – reduced levels of arousal, attention, orientation to stimuli, emotional disturbances

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48
Q

Left hemisphere deficits

A

Problems with reading, writing and understanding of speech

49
Q

Apraxia

A

inability to perform skilled movements in spite of intact sensory & motor systems.

50
Q

Agnosia

A

lesions in sensory cortices for seeing/hearing/feeling – could be one modality, can compensate using remaining modalities

51
Q

Persistent vegetative state (PVS)

A

if the link from cortex to brainstem is destroyed, eyes may open, have sleep-wake cycles and show random movements, but still unconscious and unresponsive to any stimulus

52
Q

Locked-in syndrome

A

damage to pons, opposite of PVS, cognitively fully aware w/o any mental deficits, but cannot move any body parts, except eyes and blink.

53
Q

Cerebral palsy

A

Non-progressive lesion in the brain occurring prior to 2 years of age. Can have wide spread consequences, Caused by damage to or abnormalities in the developing brain areas that disrupt movement control, posture and balance.

54
Q

Classification of cerebral palsy

A

Spastic CP (Pyramidal/corticospinal pathways), Dyskinetic CP (basal ganglia), Ataxic CP (cerebellum)

55
Q

Dyskinetic Cerebral Palsy

A

Chorea and/or athetoid-type involuntary movement problems

Dyskinesia during voluntary movement

Lack midrange motor control the most, use end range motions to accomplish tasks

Lack postural control, trunk muscle co-activation

56
Q

Cerebral Palsy etiology

A

2nd most common neurologic impairment affecting children after ASD, Exact cause/time period may be unknown, but happens due to damage to the motor control systems of the brain sometime during prenatal, perinatal or postnatal periods, often difficult to pinpoint the period of damage, low birth weight

57
Q

Cerebral palsy pathology

A

No consistent pathology

Various types of pathophysiological reasons

Mechanical trauma, metabolic problems, hypoxia, hemorrhage (injury from pressure), congenital malformations

58
Q

Cerebral palsy clinical manifestations

A

Righting reactions, protective reactions, equilibrium reactions, Persistence of primitive developmental righting reflexes – ATNR, STNR, TLR, motor control problems, spaticity in adductors and iliopsoas, weakness, oral motor problems, contractures, sensory, respiratory, GI impairments

59
Q

Righting reactions

A

used to orient head in space and align head and body
Used for developing head control and turning head/body
Integrated in 5yrs, when child starts to stand

60
Q

Protective reactions

A

Downward LE, forward UE, sideways, backward, stepping
Persists

61
Q

Equilibrium reactions

A

Allows body to maintain equilibrium by keeping COG over BOS during slow movements
Last to develop
Persists

62
Q

Prognosis of cerebral palsy

A

Most children with mild to moderate CP have normal life span, with increased mortality risks before age 4 and then after 50 years due to respiratory/CV complications
Ambulation potential can be predicted based on achievement of milestones

63
Q

Monoplegic ambulation potential

A

100%

64
Q

Hemiplegic ambulation potential

A

100%

65
Q

ataxia ambulation potential

A

100%

66
Q

Diplegia ambulation potential

A

60%-90%

67
Q

Spastic quadriplegia ambulation potential

A

0%-70%

68
Q

Sits independently by age 2 ambulation potential

A

Good

69
Q

Sits independently by age 3-4 ambulation potential

A

50% community ambulation

70
Q

Presence of primitive reflexes beyond age 2 ambulation potential

A

poor

71
Q

Absence of postural reactions beyond age 2 ambulation potential

A

poor

72
Q

independently crawled symmetrically or reciprocally by age 2.5 ambulation potential

A

Good

73
Q

Down syndrome

A

Also known as Trisomy 21, characterized by muscle hypotonia, cognitive delay, delayed development of gross motor skills, dysmorphic facial features and other distinctive physical abnormalities, rises sharply with increasing maternal age

74
Q

Down syndrome etiology

A

No known cause is yet known

75
Q

Down syndrome pathogenesis

A

Chromosomal abnormality

3 copies of chromosome 21 instead of a pair which results in a 47 chromosomes instead of 46

Extra chromosome can occur due to faulty miosis of ovum, Gene for free radical defense in chromosome 21, over expression of neurotrophic factors that are coded in chromosome 21, early onset of alziemers disease

76
Q

Down syndrome clinical manifestations

A

muscle hypotonia and joint hyper extensibility, delayed acquisition of gross motor skills, sensory impairment, obesity, diabetes, also prone to ear and respiratory infections, decreased immune function

77
Q

Down syndrome precautions

A

Activities resulting in increased forces on cervical spine may contraindicated, Lower oral motor tone can interfere with feeding, Need to educate parents. Child may need frequent feedings, clearing mucus from nose before feeds, changing child’s position frequently, postural drainage and percussion as necessary

78
Q

Neural tube defects

A

Congenital spinal canal deformities resulting from failure of neural tube closure during development

79
Q

3 types of NTDs

A

Spina Bifida Occulta

Meningocele

Myelomeningcele

80
Q

4 reasons of failure to NT to close

A

Abnormalities in hyaluronic acid matrix

Abnormal overgrowth at the caudal end stopping the closure

Abnormal production of surface ectoderm glycoproteins, that act as glue to hold the cells together during closure.

Rupture of neural tube after its closure due to CSF pressure

81
Q

Spina Bifida Occulta clinical manifestations

A

-Does not protrude visibly
-Depression/dimple on skin
-Tuft of hair present
-Soft fatty deposits underlying the skin
-Does not cause any neurologic dysfunction
-Occasional bladder/bowel disturbances and foot weakness

82
Q

Meningocele clinical manifestations

A

Like Occulta, rarely causes any neurologic deficits

83
Q

Myelomeningocele clinical manifestations

A

permanent neurologic impairment, flaccid (LMN type) paralysis, delayed postural reactions, absence of deep tendon reflexes, sensory impairments, msk deformities

84
Q

Hydrocephalus

A

increased CSF pressure due to blockage in brain or after surgical closure of myelomeningocele.

85
Q

Hydrocephalus signs/symptoms

A

Signs/symptoms include bulging soft spot (fontanel) on top of child’s head, enlargement of head, large prominent veins on scalp, setting sun sign (always looking down), seizures, vomiting, nausea, irritability, sleepiness

86
Q

Arnold-Chiari type I

A

cerebellar tonsils extend down through foramen magnum

87
Q

Arnold-Chiari type II

A

both cerebellum and brain stem extend down through foramen magnum

88
Q

Arnold-Chiari type I or Type II malformations signs/symptoms

A

weakness, vertigo, ataxia, diplopia, pain. Some people are asymptomatic
Can also cause hydrocephalus

89
Q

Tethered cord syndrome

A

Another common comorbidity following surgical closure of myelomeningocele

Spinal cord becomes ‘tethered’ or bound down resulting in progressive neurologic impairments like weakness, pain and incontinence

90
Q

Bladder and bowel incontinence with myelomenigocele

A

Always present with myelomeningocele, either small spastic bladder (urge incontinence) or large flaccid bladder (overflow incontinence = infections), can have dyssynergistic bladder

91
Q

Syringomyelia

A

Fluid-filled cavity or ‘syrinx’ present within spinal cord or brain stem – sleep apnea, choking, may require mechanical ventilation and can be fatal. Also cranial nerve involvement.

92
Q

NTD prognosis

A

Early aggressive care has improved overall prognosis, Poorest prognosis in cases of total paralysis below lesion, kyphoscoliosis, hydrocephalus, progressive loss of renal function, If child is able to ambulate or use w/c outdoors by age 7, then good prognosis for functional mobility. If it does not happen by 7-9 years, then functional ambulation might not occur.

93
Q

NTD implications for therapist

A

Pressure in sac must be avoided, prone positioning is optimal, sidelying is good for feeding or changing, with hydrocephalus, careful handling needed, avoid pressure and stretch to shunt, avoid head down positions, skin care, passive ROM and stretching

94
Q

Muscular Dystrophies

A

Largest and the most common group of inherited progressive neuromuscular disorders. Typically symmetric progressive muscle wasting with increasing deformities and disabilities

95
Q

Duchenne MD and Becker MD etiology

A

DMD most common and is x-linked recessive disorders. Males are predominantly affected with females being mostly carriers. Signs/symptoms are apparent by 2-4 years, rapidly progress, death in 20s.

BMD is slowly progressive, lifespan till adulthood, also x-linked, males mostly affected

96
Q

Limb Girdle type MD etiology

A

Autosomal genetic inheritance, many subtypes, Onset in late childhood to early adolescence, Slowly progressive and milder presentation

97
Q

Congenital MD etiology

A

Onset of symptoms at birth or shortly afterwards, Mostly autosomal recessively inherited, Severity and rate of progression varies, some die in first years, other can live longer and achieve ambulation

98
Q

Facio-Scapulo-Humeral MD etiology

A

autosomal dominant disorder, Son or daughter of affected person has 50% chance of inheriting the defective gene (males>females). Age of onset is early adolescence, slowly progressive, lifespan varies

99
Q

Myotonic Dystrophy etiology

A

autosomal dominant, often in isolated geographic locations due to local founders effect. subsequent generation shows more severe clinical presentation.

100
Q

Duchenne and Becker MD pathogenesis

A

caused by mutations of the dystrophin gene Xp21. Muscle is replaced by fatty, connective tissue and contractures develop.

101
Q

Dystrophin

A

part of the Dystrophin glycoprotein transmembrane complex, dystrophin links muscle membrane(sarcolemma) to the contractile proteins (actin/myosin). lack of normal dystrophin leads to disruption of sarcolemma during contraction-relaxation cycles, allows uncontrolled influx of Ca2+, which triggers destruction of the muscle cell.

102
Q

DMD versus BMD

A

-Males with undetectable levels of dystrophin have DMD
-Males with abnormal sized or lower levels of dystrophin have BMD

-Those who lose ambulation prior to 13 years age fall in DMD, those who walk past 16 years fall in BMD group, while those who walk past age 12 and lose that ability by 15 is defined as ‘intermediate MD’.

103
Q

Limb Girdle MD pathogenesis

A

Type 1 inherited dominantly and type 2 inherited recessively – about 20 subtypes

104
Q

Facio-Scapulo-Humeral MD pathogenesis

A

disease occurs due to expression of a protein not naturally present. Presence of reduced number of repeats produces a protein called double homeobox protein 4 (DUX4), which is normally not present.

105
Q

Myotonic Dystrophy pathogenesis

A

Underlying genetic defect is due to the phenomenon of anticipation (increasingly larger number trinucleotide repeats in subsequent generations). affects chloride channels in membrane, insulin receptors and protein tau. myotonia, risk of diabetes, cognitive delay. Muscle fibers show altered resting membrane potential

106
Q

Duchenne MD clinical manifestations

A

By 2-4 years age, muscles of shoulder girdle, rectus abdominis, pelvic girdle muscle (Gluts), start to get weak. Later distal muscles (hamstring, calf muscles). Gower’s sign, increased lumbar lordosis, Shows pseudohypertrophy of calf muscles, contractures result in toe walking. respiratory muscles get affected, cardiac muscles can also get affected

107
Q

Becker MD clinical manifestations

A

Pattern of involvement resemble DMD, but show later onset, slow progression, longer life expectancy

108
Q

Limb girdle MD clinical manifestations

A

signs are first noticed in adolescence to adulthood, affects proximal shoulder and pelvic girdle, winging of scapula, lumbar lordosis, abdominal protrusion, waddling gait, ambulation capacity varies widely

109
Q

congenital MD clinical manifestations

A

more severe, Symptoms typically present at birth, rapid loss of muscle strength and progressive respiratory symptoms

110
Q

WWS (Walker Warburg syndrome)

A

most severe CMD, presents at birth, rapidly progresses and death usually prior to 1 year age, involves ocular impairments, brain abnormalities.

111
Q

MEB (muscle eye brain) disease

A

similar clinical findings as WWS but has wider variations, retinal abnormalities, glaucoma, polymicrogyria, cerebellar abnormalities.

112
Q

Fukuyama CMD

A

onset at or shortly after birth, progressive weakness and contractures, typical loss of ambulation by 10 years age

113
Q

Facio-Scapulo-Humeral MD clinical manifestations

A

mild, onset usually 2nd decade. Inability to close eyes may be first sign, facial flattening, winging of shoulders, difficulty raising arms overhead, most people have normal lifespan

114
Q

Myotonic Dystrophy clinical manifestations

A

Typically presents with muscle weakness, wasting and myotonia (delayed relaxation of muscle following contraction)

115
Q

Myotonic Dystrophy diagnosis

A

clinical presentation, family hx, genetic testing, EMG studies show “dive-bomber” kind of sound

116
Q

MD treatment

A

No known treatment that stops progression, Use of prednisone in DMD/BMD may delay progression and allow child to walk some more years

117
Q

MD prognosis

A

Depends on the type of MD, Respiratory muscle dysfunction, cardiac muscle conduction defects are common sources of morbidity and mortality, DMD/BMD, CMD are more severe with shorter life span. People with FSHD and LGMD can expect to have relatively normal life span

118
Q

MD implications for therapist

A

Tx is directed towards maintain function for as long as possible, contracture management, encourage activity, muscle strengthening, may be contraindication, breathing ex, later stages may require airway clearance techniques

Clinical Medicine III (4 decks)

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