Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Neuroscience 2 > Clinical- 9 > Flashcards

Clinical- 9 Flashcards

1
Q

What is hemiparesis?

A

weakness on 1 side of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is hemiplegia?

A

total paralysis of 1 side of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is paraperesis?

A

weakness of the legs only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is paraplegia?

A

paralysis of the legs only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is quadiparesis?

A

weakness in all 4 limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is quadriplegia?

A

paralysis of all 4 limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is rigidity?

A

Increased resistance to passive movement throughout the range of motion. It affects agonist & antagonist muscle groups equally.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is leadpipe rigidity?

A

sustained resistance to passive movement throughout the whole range of motion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is cogwheel rigidity?

A

combination of leadpipe rigidity and tremor so it seems more jerky

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Is spasticity velocity dependent?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes spasticity?

A

UMN lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is hypotonia?

A

A reduced resistance to passive movement, excessive floppiness. It’s easier to hyperextend the joints.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is hyperreflexia?

A

Increased reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which spinal cord levels does the polysynaptic superficial abdominal reflex indicate?

A

T8-12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What causes a depressed polysynaptic superficial abdominal reflex?

A

with an upper motor neuron disturbance affecting side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What happens if there a bilateral depression of the polysynaptic superficial abdominal reflex?

A

Bilateral absent of response has no clinical significance, it can happen in the elderly, the obese, multiparous women & pts who have had ab surgery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the cremasteric reflex? ;-)

A

Retraction of the ipsilateral testis when the inner part of the thigh is lightly stroked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What nerve levels is the cremasteric reflex?

A

L1-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does a + babinski indicate?

A

Positive sign indicates upper motor neuron lesion involving the contralateral motor cortex or the corticospinal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the Sx to an UMN lesion?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the Sx to an LMN lesion?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the Sx to cerebellar dysfxn?

A 
Hypotonia
	Depressed or pendular tendon reflexes
	Ataxia (impaired coordination)
	Gait disorder
	Imbalance of station
	Disturbance of eye movement
	Dysarthria (motor problem with speaking)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the lesion in a brown sequard?

A

This is hemisection of a spinal cord @ a certain level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the Sx of a brown sequard?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are myopathic disorders?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the 4 ways u can distinguish between the different types of myopathic disorders?

A
  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
Q

What are the characteristics for neuromuscular transmission disorders?

A

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
Q

Serum concentrations of which enzyme is the best for following the course of muscle disease?

A

CK

39
Q

What test can u run to see whether the weakness if neurogenic or myopathic in origin?

A

muscle biopsy

40
Q

What will a neurogenic disorder show on muscle biopsy?

A

group atrophy, with large fibers surrounding it (unaffected muscle fibers)

41
Q

What will a myopathic disorder show on muscle biopsy?

A

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
Q

What causes traumatic myelopathy?

A

damage to the spinal cord from either whiplash injury, fracture-dislocation in the cervical, lower thoracic or upper lumbar region

43
Q

What occurs during the acute stage of traumatic myelopathy?

A

flaccid paralysis with loss of tendon and other reflexes. Sensory loss and urinary & fecal retention

44
Q

What occurs during the following weeks with traumatic myelopathy?

A

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
Q

What are the initial treatments for traumatic myelopathy?

A

Immobilization and Corticosteroids

46
Q

What do u give with painful flexor or extensor spasms?

A

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
Q

MS- epidemiology

A

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
Q

MS- mutation

A

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
Q

MS- pathophysiology

A

The cause of MS is unknown but it results in our own immune system attacking the myelin antigen.

50
Q

MS- initial Sx

A

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
Q

MS- advanced Sx

A 
Absent Ab reflexes
Hyper reflex
\+ Babinski sign
Nystagmus
Gait
52
Q

What form of MS is the most common (85%) in which progression does not occur between attacks?

A

Relapsing remitting form

53
Q

What form of MS has a gradually progressive course after an initial relapsing remitting pattern?

A

Secondary progressive form

54
Q

What form of MS has a gradual progression of disability from clinical onset?

A

Primary progressive form

55
Q

MS- Dx

A

MS needs at least two different regions of the central white matter to have been affected at different times

56
Q

You need 3/4 of what features to confirm a MS Dx?

A
  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
Q

You need 2/3 of what features to confirm a primary progressive disease of MS?

A
  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
Q

What drug can u give for MS to prevent relapses?

A

Interferon β-1a or interferon β-1b

59
Q

What drug can be Given if there is no benefit with Interferon βs, and is given by daily subcutaneous injection?

A

Glatiramer acetate

60
Q

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?

A

Natalizumab

61
Q

When can plasmaphaeresis help MS pts?

A

sometimes helpful when patients have severe relapses that are unresponsive to steroids

62
Q

When can corticosteroids help MS pts?

A

Intravenous methylprednisolone Treatment of choice for acute relapses

63
Q

MS- prognosis

A

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
Q

Acute Disseminated Encephalomyelitis (ADE)- epidemiology

A

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
Q

ADE- clinical findings

A

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
Q

ADE- Tx

A

Corticosteroids are prescribed but doesn’t really benefit

IV immunoglobulin or plasmaphereisis is sometimes helpful

67
Q

ADE- prognosis

A

mortality rate is 5-30%

68
Q

Which bug is causes the most epidural abscesses?

A

Staphylococcus aureus

69
Q

Epidural abscesses- clinical findings

A 
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
Q

Epidural abscesses- Dx (scans, labs, csf)

A

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
Q

Epidural abscesses- Tx

A

Surgery & Ab
Nafcillin/ vancomycin: covers Staph or strep infection
Ceftazidime/cefpime (3-4th generation cephalosporin): gram neg infection

72
Q

Tetanus- MOA

A

The toxin interrupts the release of glycine & GABA (inhibitory neurotransmitters) causing motor nerve hyperactivity

73
Q

Tetanus- Sx

A

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
Q

Tetanus- Dx

A

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
Q

Tetanus- prevention

A

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
Q

Tetanus- Tx

A

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
Q

What causes anterior spinal artery syndrome?

A 
Trauma
Dissection aortic aneurysm
Aortography
Polyarteritis nodosa
Hypotensive crisis
78
Q

What are the acute findings for ASA syndrome?

A

Acute onset of a flaccid, areflexic paraparesis (spinal shock)

79
Q

What are the prolonged findings for ASA syndrome?

A

Spastic paraparesis with brisk tendon reflexes & + Babinski sign
Pain & temp gone
Post column still intact (vibration & proprioception ok)

80
Q

Cerivcal spondylosis- Sx

A

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
Q

Cerivcal spondylosis- cause

A

Chronic cervical disk degeneration
With herniation of disk material
Secondary calcification
Associated osteophytic outgrowth

82
Q

Cerivcal spondylosis- usual affected roots

A

C5-6 (weakness of deltoid, supra & infra spinatus, biceps, bachioradialis. Depressed bicep & brachioradialis reflex)

83
Q

Cerivcal spondylosis- Tx

A 
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
84
Q

What are the 2 intramedullary tumors (10%) that cause cord compression?

A

ependymomas and gliomas

85
Q

What are the 6 extramedullary tumors (90%) that cause cord compression?

A

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
Q

What are the Sx for comrpession of the spinal cord from tumors?

A

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
Q

How do u Dx a tumor that compresses the spinal cord? (scans and CSF)

A

CSF is xanthochromic (yellowish CSF) with a greatly increased protein concentration
CT, MRI or myelography is necessary

88
Q

How do u Tx a tumor that compresses the spinal cord?

A

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
Q

What is the prognosis of a tumor that compresses the spinal cord?

A

Depends on the cause and severity before it is relieved

Extradural metastasis: can cause permanent impairment of motor, sensory and sphincter function

Clinical Neuroscience 2 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions