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Adult Neuro > Cranial and Peripheral Nerve Disorders and Other Central Nervous System Disorders > Flashcards

Cranial and Peripheral Nerve Disorders and Other Central Nervous System Disorders Flashcards

1
Q

Wallerian degeneration

A

transection results in degeneration of the axon and myelin sheath distal to the site of axonal interruption

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2
Q

Axonal degeneration

A

degeneration of axon cylinder and myelin, progressing from distal to proximal, “dying back” of nerves (peripheral neuropathy

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3
Q

Basic Pathological Process:

A

Wallerian degeneration
segmental demyelination
axonal degeneration

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4
Q

Neuropathy (peripheral neuropathy):

A

any disease of nerves characterized by deteriorating neural function (diabetic neuropathy)

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5
Q

Polyneuropathy

A

bilateral symmetrical involvement of PNs, usually more legs than arms, distal segments earlier and more involved than proximal

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6
Q

Radiculopathy

A

involvement of nerve roots

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7
Q

Neurapraxia (class 1)

A

injury to nerve that causes a transient loss of function (conduction block ischemia); typically resolves rapidly or persists only a few weeks

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8
Q

Axonotmesis (Class 2):

A

injury to nerve disrupting the axon and causing loss of function and Wallerian degeneration distal to the lesion with no disruption of the endoneurium, regeneration is possible

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9
Q

Neurotmesis (Class 3):

A

cutting of the nerve with severance of all structures and complete loss of function; re-nnervation typically fails without surgical intervention

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10
Q

Clinical Symptoms of LMN Syndrome:

A

Weakness/paresis of denervated muscle, hyporeflexia and hypotonia, atrophy, fatigue
sensory loss
muscle pain
ANS dysfunction
Hyper excitability of remaining nerve fibers

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11
Q

NCV Studies:

A

conduction times (motor, sensory) are slowed or complete conduction block may be evident

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12
Q

EMG (motor nerve function)

A

examine for signs of widespread denervation atrophy (spontaneous fibrillation potentials); evidence of re-innervation (low amplitude, short duration, poly-phasic motor unit potentials)

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13
Q

What is the etiology of trigeminal neuralgia?

A

Results from degeneration (etiology unknown) or compression (tortuous basilar artery or cerebellopontine tumor)
Occurs in older population (mean age 50)
Abrupt onset

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14
Q

What are characteristics of trigeminal neuralgia?

A

brief paroxysms of neurogenic pain (stabbing/shooting), reoccurring frequently

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15
Q

Where does trigeminal neuralgia occur?

A

along the distribution of the trigeminal nerve, mandibular and maxillary divisions (involvement of ophthalmic division in rare)
one side of face

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16
Q

What exacerbates and relieves trigeminal neuralgia?

A

stress and relaxation

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17
Q

Trigger points of trigeminal neuralgia?

A

Trigger points: light touch to face, lips, or gums will cause pain
Triggering stimuli: extremes of heat or cold, chewing, talking, brushing teeth, movement of air across face

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18
Q

Etiology of Bell’s Palsy:

A

acute inflammatory process of unknown etiology (immune or viral disease) resulting in compression of the nerve within the temporal bone

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19
Q

Characteristics of Bell’s Palsy:

A

Muscles of facial expression on one side are weakened/paralyzed
Loss of control of salivation or lacrimation
Onset is acute, with maximum severity in a few hours or days
Commonly preceded by a day or 2 of pain behind the ear

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20
Q

Exam of Bell’s Palsy:

A

Drooping of corner of mouth, eyelids that don’t close
Function of muscles of facial expression (test CN VII)
Taste of anterior 2/3 of tongue

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21
Q

PT goals for Bell’s Palsy:

A

Protect cornea (artificial tears or patching) until recovery allows for eyelid closure
E-stim to maintain tone, support of function of facial mm
Provide active facial muscle exercises
Functional retraining: chewing

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22
Q

Bulbar Palsy (bulbar paralysis):

A

Refers to weakness or paralysis of the muscles innervated by the motor nuclei of the lower brainstem, affecting the muscles of the face, tongue, larynx and pharynx

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23
Q

Etiology of Bulbar Palsy:

A

result of tumors, vascular or degenerative diseases of lower cranial nerve motor nuclei (ALS)

24
Q

Examof Bulbar Palsy:

A

Glossopharyngeal and Vagal Paralysis
Phonation, articulation, palatal action, gag reflex, swallowing
Changes in voice quality: dysphonia (hoarseness or nasal quality)
Bilateral involvement: severe airway restriction with dyspnea, difficulty with coughing

25
Q

Pseudobulbar Palsy

A

Bilateral dysfunction of corticobulbar innervation of brainstem nuclei
A central UMN lesion analogous to corticospinal lesions disrupting function of anterior horn cells

26
Q

Symptoms of Pseudobulbar Palsy:

A

Produces similar symptoms of bulbar palsy

Examine for hyperactive reflexes: increased jaw jerk and snout reflex ( tapping on lips produces pouting of lips)

27
Q

Signs and Symptoms of AIDS:

A

HA, diarrhea, nausea, vomiting, fatigue, aching muscles, sore throat, red rash that does not itch—flu-like symptoms last 2-4 wks, confusion, forgetfulness, behavioral changes, loss of sensation in extremities, atrophy

28
Q

Alcoholic Ataxia:

A

A loss of coordination in performing voluntary movements associated with peripheral neuritis as a result of alcoholism

29
Q

Signs and Symptoms of Alcoholic Ataxia:

A

Wide-footed, unsteady gait
slurred speech
clumsiness of their hands
double vision,
legs often affected pt. states “slow legs”
peripheral neuropathy (especially in feet and legs)
loss in vibration sense and DTR

30
Q

Exam for Alcoholic Ataxia:

A 
Romberg sign
finger to nose test
gait assessment (tandem gait)
sensory testing
DTR
MMT to rule out weakness
31
Q

Patient Management for Alcoholic Ataxia:

A

improve balance and postural reactions against external stimuli and gravitational
increases postural stabilization following joint stabilization
developing UE function
develop independent functional gait

32
Q

Neocerebellar Lesions (Posterior):

A

Ipsilateral ataxia, Ipsilateral hypotonia & hyporeflexia, Dysmetria, Adiadochkinesia, movement decomposition, asthenia, intention tremors, rebound phenomenon, ataxic gait, staccato voice

33
Q

Paleocerebellar Lesions (Anterior):

A

Disturbances in extensor tone (b/c this lobe receives the Spinocerebellar tracts – which when lost result in an ↑ in extensor tone.

34
Q

Archicerebellar Lesions (Flocculonodular):

A

Uncoordinated trunk movements – ataxia. Balance deficits d/t loss of vestibular input from vestibular nuclei, cuneocerebellar tract, and rostral cerebellar tract

35
Q

PT/OT for cerebellar dysfunction:

A

Added weight to help decrease tremor; but performance declines due to the added weight
Strengthening (help with deconditioning, weakness, or spasticity)

36
Q

Speech for cerebellar dysfunction:

A

Swallowing exercises , dietary modification
Feeding by percutaneous endoscopic gastrostomy (PEG) tube
In advanced cases: feeding via PEG tube can reduce risk of aspiration

37
Q

Cerebellar Dysfunction signs:

A 
hypotonicity
asthenia
ataxia
Dysmetria, Gait Disturbance, Movement Decomposition
Dysdiadochokinesia, Speech, Eye Movement
38
Q

Myasthenia Gravis:

A

A neuromuscular junction disorder characterized by progressive muscular weakness and fatigability on exertion

39
Q

Etiology of Myasthenia gravis:

A

autoimmune antibody-mediated attack on acetylcholine receptors at neuromuscular junction

40
Q

Characteristics of Myasthenia Gravis:

A

Muscular strength worse with continuing contraction, improved with rest

41
Q

4 types of Myasthenia Gravis:

A

Ocular myasthenia
Mild generalized myasthenia
Severe generalized myasthenia
crisis

42
Q

Generalized myasthenia

A

usually involves bulbar (extraocular, facial and muscles of mastication) and proximal limb girdle muscles
may progress from mild to severe within 18 month

43
Q

Myasthenic crisis

A

myasthenia gravis with respiratory failure; treat as medical emergency

44
Q

Myasthenia Gravis exam:

A

Cranial nerves: examine for diploplia, ptosis, progressive dysarthria or nasal speech, difficulty in chewing and swalling, difficulties in facial expression, drooping facial mm Respiratory function

45
Q

Which muscles are more involved in myasthenia gravis?

A

proximal more involved than distal, fatigability, repeated muscle use results in rapid weakness

46
Q

Signs and Symptoms of Brian Tumor:

A 
Headaches (usually worse in the morning)
Nausea and vomiting
Changes in speech, vision, or hearing
Problems balancing or walking
Changes in mood, personality, or ability to concentrate
Problems with memory
Muscle jerking or twitching (seizures or convulsions)
Numbness or tingling in the arms or legs
47
Q

Grade I Tumor:

A

The tissue is benign. The cells look nearly like normal brain cells, and they grow slowly.

48
Q

Grade II Tumor:

A

The tissue is malignant. The cells look less like normal cells than do the cells in a Grade I tumor

49
Q

Grade III Tumor:

A

The malignant tissue has cells that look very different from normal cells. The abnormal cells are actively growing

50
Q

Grade IV Tumor:

A

The malignant tissue has cells that look most abnormal and tend to grow quickly

51
Q

Astrocytoma:

A

The tumor arises from star-shaped glial cells called astrocytes. It can be any grade. In adults, an astrocytoma most often arises in the cerebrum

52
Q

Meningioma:

A

The tumor arises in the meninges. It can be grade I, II, or III. It’s usually benign (grade I) and grows slowly

53
Q

Oligodendroglia

A

The tumor arises from cells that make the fatty substance that covers and protects nerves. It usually occurs in the cerebrum. It’s most common in middle-aged adults. It can be grade II or III

54
Q

Signs and Symptoms of Abscess:

A

symptoms are present for less than 2 wks
Dependent on size and location of the lesion
Often present with fever, HA, and focal neurological deficits
Changes in mental status due to cerebral edema, nausea vomiting, neck stiffness

55
Q

Abscess Exam:

A 
ataxia, 
papilledema
general or focal seizures
drowsiness
hemiparesis
slurred speech

Adult Neuro (26 decks)

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