Clinical- 9 Flashcards
1
Q
What is hemiparesis?
A
weakness on 1 side of the body
2
Q
What is hemiplegia?
A
total paralysis of 1 side of the body
3
Q
What is paraperesis?
A
weakness of the legs only
4
Q
What is paraplegia?
A
paralysis of the legs only
5
Q
What is quadiparesis?
A
weakness in all 4 limbs
6
Q
What is quadriplegia?
A
paralysis of all 4 limbs
7
Q
What is the 0-5 grading scale for muscle strength?
A
5- normal
4- Active movement against resistance & gravity
3- Active movement against gravity but not resistance
2- Active movement possible only without gravity
1- Flicker or trace of contraction
0- No contraction
8
Q
What are the drugs that can cause myopathy?
A
β-blocker Cholorquine Clofibrate Corticosteroids Drugs causing hypokalemia Emetine ε-aminocaproic acid HMG-CoA reductase inhibitor Penicillamine Zidovudine
9
Q
What is rigidity?
A
Increased resistance to passive movement throughout the range of motion. It affects agonist & antagonist muscle groups equally.
10
Q
What does rigidity indicate?
A
Indicates extrapyramidal dysfunction (problem w/ involuntary movements & coordination) and is to a lesion of the basal ganglia. Not dependent on the speed of the movement.
11
Q
What is leadpipe rigidity?
A
sustained resistance to passive movement throughout the whole range of motion
12
Q
What is cogwheel rigidity?
A
combination of leadpipe rigidity and tremor so it seems more jerky
13
Q
What is spasticity?
A
Increase in muscle tone. In the arm: flexor muscle tones are more increased. In the legs: extensor muscle tones are more increased.
14
Q
Is spasticity velocity dependent?
A
Yes
15
Q
What causes spasticity?
A
UMN lesion
16
Q
What is hypotonia?
A
A reduced resistance to passive movement, excessive floppiness. It’s easier to hyperextend the joints.
17
Q
What does hypotonia indicate?
A
It is associated with lower motor neuron problem, primary muscle disorders, disruption of the sensory (afferent) limb of the reflex arc, cerebellar disease and certain extrapyramidal disorders such as Huntington disease, as well as in the acute stage of a pyramidal lesion (upper motor lesion)
18
Q
What is areflexia?
A
Loss of the tendon reflexes by any lesion that interrupts the structural or functional continuity of its reflex arc, as in a root lesion or peripheral neuropathy
19
Q
What does areflexia indicate?
A
Reflexes are more depressed during the acute stage of upper motor neuron lesion. Remember to do Jerdrassik maneuver to make sure that the reflex is really absent (this is when the pt pull apart the fingers of two hands when they are hooked together)
20
Q
What is hyperreflexia?
A
Increased reflex
21
Q
What does hyperreflexia indicate?
A
Occurs with upper motor neuron lesions but it can happen with symmetric distribution in certain healthy patient and in patients under emotion tension so look for reflex asymmetry
22
Q
What is clonus?
A
Series of rhythmic reflex contractions and relaxation of a muscle that occurs after sustained stretch. From upper motor neuron lesion
23
Q
What is the normal response to the polysynaptic superficial abdominal reflex?
A
A normal response would be contraction of the muscle in the quadrant stimulated with brief movement of the umbilicus toward the stimulus
24
Q
Which spinal cord levels does the polysynaptic superficial abdominal reflex indicate?
A
T8-12
25
What causes a depressed polysynaptic superficial abdominal reflex?
with an upper motor neuron disturbance affecting side
26
What happens if there a bilateral depression of the polysynaptic superficial abdominal reflex?
Bilateral absent of response has no clinical significance, it can happen in the elderly, the obese, multiparous women & pts who have had ab surgery.
27
What is the cremasteric reflex? ;-)
Retraction of the ipsilateral testis when the inner part of the thigh is lightly stroked
28
What nerve levels is the cremasteric reflex?
L1-2
29
What does a + babinski indicate?
Positive sign indicates upper motor neuron lesion involving the contralateral motor cortex or the corticospinal tract
30
What are the Sx to an UMN lesion?
Weakness or paralysis (usually in the beginning)
Spasticity
Increased tendon reflexes/ hyper reflex
An extensor plantar response (positive Babinski sign)
Loss of superficial ab reflexes
Little to no muscle atrophy
31
What are the Sx to an LMN lesion?
Weakness or paralysis
Wasting & fasciculation of involved muscles
Hypotonia (flaccidity)
Loss of tendon reflexes when neuron subserving them are affected
Normal ab & negative babinski sign (plantar flexion)- unless the neurons subserving them are directly involved then reflexes are lost.
32
What are the Sx to cerebellar dysfxn?
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Hypotonia
Depressed or pendular tendon reflexes
Ataxia (impaired coordination)
Gait disorder
Imbalance of station
Disturbance of eye movement
Dysarthria (motor problem with speaking)
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33
What is the lesion in a brown sequard?
This is hemisection of a spinal cord @ a certain level
34
What are the Sx of a brown sequard?
Ipilateral side of that spinal cord segment will lose all sensation
Ipilateral impairment of vibration and positional sense below that level (posterior column gone)
Contralateral loss of pain and temperature (ALS gone- From Dr. K, its couple levels below the lesion)
35
What are myopathic disorders?
Weakness, usually proximally than distally
No muscle wasting or depression of tendon reflexes until advanced stage
Normal ab & plantar reflex (- Babinski sign)
No sensory loss or sphincter disturbances
36
What are the 4 ways u can distinguish between the different types of myopathic disorders?
1. Determine whether the weakness is congenital or acquired
2. Is there a family history of similar disorder
3. Is there any clinical evidence that a systemic disease may be responsible
4. Distribution of affected muscle
37
What are the characteristics for neuromuscular transmission disorders?
Normal or reduced muscle tone
Normal or depressed tendon & superficial reflexes
No sensory change
Weakness, often patchy in distribution, not conforming to the distribution of any single anatomic structure; frequently involves the cranial muscle and may fluctuate in severity over short periods, particularly in relation to activity
Disease to either the pre or postsynaptic portion of the NMJ may impair NM transmission
38
Serum concentrations of which enzyme is the best for following the course of muscle disease?
CK
39
What test can u run to see whether the weakness if neurogenic or myopathic in origin?
muscle biopsy
40
What will a neurogenic disorder show on muscle biopsy?
group atrophy, with large fibers surrounding it (unaffected muscle fibers)
41
What will a myopathic disorder show on muscle biopsy?
atrophy occurs in a random pattern, nuclei of muscle cells may be centrally situated (normally they are peripherally situated) and fibrosis or fatty infiltration may be seen
42
What causes traumatic myelopathy?
damage to the spinal cord from either whiplash injury, fracture-dislocation in the cervical, lower thoracic or upper lumbar region
43
What occurs during the acute stage of traumatic myelopathy?
flaccid paralysis with loss of tendon and other reflexes. Sensory loss and urinary & fecal retention
44
What occurs during the following weeks with traumatic myelopathy?
reflex returns but becomes brisk and + Babinski sign
Spastic paraplegia or quadriplegia. At the level of the lesion where the anterior horn is damaged will have flaccid, atrophic paralysis of the muscle (lower motor neuron). Bladder & bowel have regained some reflex function and they are expelled at intervals.
45
What are the initial treatments for traumatic myelopathy?
Immobilization and Corticosteroids
46
What do u give with painful flexor or extensor spasms?
Baclofen, diazepam: Enhance spinal inhibitory mechanism. Side effects include dryness of the mouth, somnolence (drowsiness) & hypotension
Dantrolene: uncouple muscle excitation from contraction. It may also increase weakness and should be avoided in pt with severely compromised respiratory function
47
MS- epidemiology
It’s one of the most common neurological disorder and its highest incidence is in young adults. Affects women twice more often than men. Involvement of different parts of the CNS at different times
48
MS- mutation
There is a genetic predisposition with strong association between the diseases and HLA DR2 antigens. Alleles of IL2RA (interleukin-2 receptor α gene) and IL7RA (interleukin-7 receptor α gene) is also heritable risk factor for MS.
49
MS- pathophysiology
The cause of MS is unknown but it results in our own immune system attacking the myelin antigen.
50
MS- initial Sx
Focal weakness, numbness, tingling (paresthesia) or unsteadiness in a limb
Sudden loss or burring of vision in one eye (optic neuritis)
Diplopia (double vision)
Disequilibrium
Bladder function disturbance (urinary urgency or hesitancy)
51
MS- advanced Sx
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Absent Ab reflexes
Hyper reflex
+ Babinski sign
Nystagmus
Gait
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52
What form of MS is the most common (85%) in which progression does not occur between attacks?
Relapsing remitting form
53
What form of MS has a gradually progressive course after an initial relapsing remitting pattern?
Secondary progressive form
54
What form of MS has a gradual progression of disability from clinical onset?
Primary progressive form
55
MS- Dx
MS needs at least two different regions of the central white matter to have been affected at different times
56
You need 3/4 of what features to confirm a MS Dx?
1. At least one gadolinium enhancing lesion or nine T2 hyper intense lesion if there is no enhancing lesion
2. One or more infratentorial (cerebellar) lesion
3. One or more juxtacortical (near the cortex) lesion
4. At least three periventricular lesions
57
You need 2/3 of what features to confirm a primary progressive disease of MS?
1. Positive MRI (nine T2 lesions or at least four T2 lesion with an abnormal visual evoked potential)
2. Two or more focal T2 lesions on spinal MRI
3. Positive CSF (oligoclonal bands, increased IgG index or both)
58
What drug can u give for MS to prevent relapses?
Interferon β-1a or interferon β-1b
59
What drug can be Given if there is no benefit with Interferon βs, and is given by daily subcutaneous injection?
Glatiramer acetate
60
What is the Drug of choice for lesions with very high disease activity (multiple gadolinium enhancing lesions on MRI) or if the disease progresses or remains poorly controlled?
Natalizumab
61
When can plasmaphaeresis help MS pts?
sometimes helpful when patients have severe relapses that are unresponsive to steroids
62
When can corticosteroids help MS pts?
Intravenous methylprednisolone Treatment of choice for acute relapses
63
MS- prognosis
some degree of disability will happen eventually but about half of all pts are only mildly or moderately disabled 10years after the onset of symptoms
64
Acute Disseminated Encephalomyelitis (ADE)- epidemiology
Occurs as a single episode of neurologic symptoms
Symptoms progress over few days in associate with a viral infection (esp measles or chickenpox)
Perivascular areas of demyelination are scattered throughout the brain & spinal cord with an associated inflammatory reaction
More common in children
65
ADE- clinical findings
Meningeal irritation
Flaccid weakness and sensory disturbance of the legs
+ Babinski sign
Urinary retention
There may be involvement of optic N, cerebral hemisphere, brainstem or cerebellum
Lesions in white matter, optic N, basal ganglion, thalamus, cerebellum, brainstem or spinal cord.
66
ADE- Tx
Corticosteroids are prescribed but doesn’t really benefit
| IV immunoglobulin or plasmaphereisis is sometimes helpful
67
ADE- prognosis
mortality rate is 5-30%
68
Which bug is causes the most epidural abscesses?
Staphylococcus aureus
69
Epidural abscesses- clinical findings
```
Fever, headache & malaise
Backache & tenderness
Pain in the distribution of a spinal N root
Rapidly progressive paraparesis
Sensory disturbances in the legs
Urinary & fecal retention
```
70
Epidural abscesses- Dx (scans, labs, csf)
MRI with gadolinium enhancement is used to look for abscess
Lab will show peripheral leukocytosis and increased erythrocyte sedimentation rate (measures how much inflammation is in the body)
CSF will show mild pleocytosis (↑ cell count) w/ increase protein but normal glucose concentration
71
Epidural abscesses- Tx
Surgery & Ab
Nafcillin/ vancomycin: covers Staph or strep infection
Ceftazidime/cefpime (3-4th generation cephalosporin): gram neg infection
72
Tetanus- MOA
The toxin interrupts the release of glycine & GABA (inhibitory neurotransmitters) causing motor nerve hyperactivity
73
Tetanus- Sx
Trimus (lockjaw)
Difficulty in swallowing or spasm of the facial muscle that resembles a contorted smile (risus sardonicus)
Painful muscle spasms & rigidity progress to involve both trunk & limb muscles and may give rise to hyperextended posturing (Opisthotons)
74
Tetanus- Dx
Continuous motor unit activity
Absence of the normal silent period in the masseter muscle following elicitation of the jaw-jerk reflex
Elevated serum CK & myoglobinuria
Culture of the organism
75
Tetanus- prevention
Immunization with tetanus toxoid
Debridement of wounds
Pt w/ open wound will get additional dose of tetanus toxoid if they didn’t get the booster dose within 10years
76
Tetanus- Tx
Tetanus immune globulin to neutralize the toxin (Intrathecal admin)
Penicillin/ metronidazole for the infection
Chlorpromazine, Diazepam & Baclofen: for treating painful spasms and rigidity
If these fail then use neuromuscular blockade w/ vecuronium/pancuronium
77
What causes anterior spinal artery syndrome?
```
Trauma
Dissection aortic aneurysm
Aortography
Polyarteritis nodosa
Hypotensive crisis
```
78
What are the acute findings for ASA syndrome?
Acute onset of a flaccid, areflexic paraparesis (spinal shock)
79
What are the prolonged findings for ASA syndrome?
Spastic paraparesis with brisk tendon reflexes & + Babinski sign
Pain & temp gone
Post column still intact (vibration & proprioception ok)
80
Cerivcal spondylosis- Sx
Pain & stiffness in the neck
Pain in the arms with or without a segmental motor or sensory deficit in the arms
Upper motor neuron deficit in the legs
81
Cerivcal spondylosis- cause
Chronic cervical disk degeneration
With herniation of disk material
Secondary calcification
Associated osteophytic outgrowth
82
Cerivcal spondylosis- usual affected roots
C5-6 (weakness of deltoid, supra & infra spinatus, biceps, bachioradialis. Depressed bicep & brachioradialis reflex)
83
Cerivcal spondylosis- Tx
```
Cervical collar to restrict neck movements
Analgesics
NSAID
Muscle relaxants
Tricyclic drugs
Anticonvulsant
Physical therapy
Surgery if there is significant neurologic deficit, root pain is severe, persistent and unresponsive to conservative measures
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84
What are the 2 intramedullary tumors (10%) that cause cord compression?
ependymomas and gliomas
85
What are the 6 extramedullary tumors (90%) that cause cord compression?
a. Extradural
i. Carcinomatous metastases (esp from bronchus, breast or prostate)
ii. Lymphomatous
iii. Leukemic deposits
iv. Myeloma
v. Neurofibromas & meningiomas
b. Intradural
i. Neurofibromas & meningiomas
86
What are the Sx for comrpession of the spinal cord from tumors?
Symptoms are rapid if it’s from metastatic carcinoma
Pain (main)
W/extradural lesion: pain is radicular, localized to the back or it’s diffused in an extremity. It is aggravated by coughing or straining
Motor symptoms: weakness, focal wasting, heaviness, stiffness
87
How do u Dx a tumor that compresses the spinal cord? (scans and CSF)
CSF is xanthochromic (yellowish CSF) with a greatly increased protein concentration
CT, MRI or myelography is necessary
88
How do u Tx a tumor that compresses the spinal cord?
Analgesics
Corticosteroids
Radiotherapy
Hormonal treatment
Decompressive laminectomy (not usually needed)
Extramedullary-Intradural lesion are best removed
Intramedullary tumors are decompressed and surgically excised when possible and it is also treated with radiotherapy.
89
What is the prognosis of a tumor that compresses the spinal cord?
Depends on the cause and severity before it is relieved
| Extradural metastasis: can cause permanent impairment of motor, sensory and sphincter function
