Cranial and Peripheral Nerve Disorders and Other Central Nervous System Disorders

Question 1

Wallerian degeneration

Answer 1

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

Question 2

Axonal degeneration

Answer 2

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

Question 3

Basic Pathological Process:

Answer 3

Wallerian degeneration
segmental demyelination
axonal degeneration

Question 4

Neuropathy (peripheral neuropathy):

Answer 4

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

Question 5

Polyneuropathy

Answer 5

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

Question 6

Radiculopathy

Answer 6

involvement of nerve roots

Question 7

Neurapraxia (class 1)

Answer 7

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

Question 8

Axonotmesis (Class 2):

Answer 8

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

Question 9

Neurotmesis (Class 3):

Answer 9

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

Question 10

Clinical Symptoms of LMN Syndrome:

Answer 10

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

Question 11

NCV Studies:

Answer 11

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

Question 12

EMG (motor nerve function)

Answer 12

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

Question 13

What is the etiology of trigeminal neuralgia?

Answer 13

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

Question 14

What are characteristics of trigeminal neuralgia?

Answer 14

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

Question 15

Where does trigeminal neuralgia occur?

Answer 15

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

Question 16

What exacerbates and relieves trigeminal neuralgia?

Answer 16

stress and relaxation

Question 17

Trigger points of trigeminal neuralgia?

Answer 17

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

Question 18

Etiology of Bell’s Palsy:

Answer 18

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

Question 19

Characteristics of Bell’s Palsy:

Answer 19

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

Question 20

Exam of Bell’s Palsy:

Answer 20

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

Question 21

PT goals for Bell’s Palsy:

Answer 21

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

Question 22

Bulbar Palsy (bulbar paralysis):

Answer 22

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

Question 23

Etiology of Bulbar Palsy:

Answer 23

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

Question 24

Examof Bulbar Palsy:

Answer 24

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

Question 25

Pseudobulbar Palsy

Answer 25

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

Question 26

Symptoms of Pseudobulbar Palsy:

Answer 26

Produces similar symptoms of bulbar palsy | Examine for hyperactive reflexes: increased jaw jerk and snout reflex ( tapping on lips produces pouting of lips)

Question 27

Signs and Symptoms of AIDS:

Answer 27

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

Question 28

Alcoholic Ataxia:

Answer 28

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

Question 29

Signs and Symptoms of Alcoholic Ataxia:

Answer 29

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

Question 30

Exam for Alcoholic Ataxia:

Answer 30

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

Question 31

Patient Management for Alcoholic Ataxia:

Answer 31

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

Question 32

Neocerebellar Lesions (Posterior):

Answer 32

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

Question 33

Paleocerebellar Lesions (Anterior):

Answer 33

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

Question 34

Archicerebellar Lesions (Flocculonodular):

Answer 34

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

Question 35

PT/OT for cerebellar dysfunction:

Answer 35

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

Question 36

Speech for cerebellar dysfunction:

Answer 36

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

Question 37

Cerebellar Dysfunction signs:

Answer 37

``` hypotonicity asthenia ataxia Dysmetria, Gait Disturbance, Movement Decomposition Dysdiadochokinesia, Speech, Eye Movement ```

Question 38

Myasthenia Gravis:

Answer 38

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

Question 39

Etiology of Myasthenia gravis:

Answer 39

autoimmune antibody-mediated attack on acetylcholine receptors at neuromuscular junction

Question 40

Characteristics of Myasthenia Gravis:

Answer 40

Muscular strength worse with continuing contraction, improved with rest

Question 41

4 types of Myasthenia Gravis:

Answer 41

Ocular myasthenia Mild generalized myasthenia Severe generalized myasthenia crisis

Question 42

Generalized myasthenia

Answer 42

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

Question 43

Myasthenic crisis

Answer 43

myasthenia gravis with respiratory failure; treat as medical emergency

Question 44

Myasthenia Gravis exam:

Answer 44

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

Question 45

Which muscles are more involved in myasthenia gravis?

Answer 45

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

Question 46

Signs and Symptoms of Brian Tumor:

Answer 46

``` 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 ```

Question 47

Grade I Tumor:

Answer 47

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

Question 48

Grade II Tumor:

Answer 48

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

Question 49

Grade III Tumor:

Answer 49

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

Question 50

Grade IV Tumor:

Answer 50

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

Question 51

Astrocytoma:

Answer 51

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

Question 52

Meningioma:

Answer 52

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

Question 53

Oligodendroglia

Answer 53

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

Question 54

Signs and Symptoms of Abscess:

Answer 54

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

Question 55

Abscess Exam:

Answer 55

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