Cranial and Peripheral Nerve Disorders and Other Central Nervous System Disorders Flashcards
Wallerian degeneration
transection results in degeneration of the axon and myelin sheath distal to the site of axonal interruption
Axonal degeneration
degeneration of axon cylinder and myelin, progressing from distal to proximal, “dying back” of nerves (peripheral neuropathy
Basic Pathological Process:
Wallerian degeneration
segmental demyelination
axonal degeneration
Neuropathy (peripheral neuropathy):
any disease of nerves characterized by deteriorating neural function (diabetic neuropathy)
Polyneuropathy
bilateral symmetrical involvement of PNs, usually more legs than arms, distal segments earlier and more involved than proximal
Radiculopathy
involvement of nerve roots
Neurapraxia (class 1)
injury to nerve that causes a transient loss of function (conduction block ischemia); typically resolves rapidly or persists only a few weeks
Axonotmesis (Class 2):
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
Neurotmesis (Class 3):
cutting of the nerve with severance of all structures and complete loss of function; re-nnervation typically fails without surgical intervention
Clinical Symptoms of LMN Syndrome:
Weakness/paresis of denervated muscle, hyporeflexia and hypotonia, atrophy, fatigue
sensory loss
muscle pain
ANS dysfunction
Hyper excitability of remaining nerve fibers
NCV Studies:
conduction times (motor, sensory) are slowed or complete conduction block may be evident
EMG (motor nerve function)
examine for signs of widespread denervation atrophy (spontaneous fibrillation potentials); evidence of re-innervation (low amplitude, short duration, poly-phasic motor unit potentials)
What is the etiology of trigeminal neuralgia?
Results from degeneration (etiology unknown) or compression (tortuous basilar artery or cerebellopontine tumor)
Occurs in older population (mean age 50)
Abrupt onset
What are characteristics of trigeminal neuralgia?
brief paroxysms of neurogenic pain (stabbing/shooting), reoccurring frequently
Where does trigeminal neuralgia occur?
along the distribution of the trigeminal nerve, mandibular and maxillary divisions (involvement of ophthalmic division in rare)
one side of face
What exacerbates and relieves trigeminal neuralgia?
stress and relaxation
Trigger points of trigeminal neuralgia?
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
Etiology of Bell’s Palsy:
acute inflammatory process of unknown etiology (immune or viral disease) resulting in compression of the nerve within the temporal bone
Characteristics of Bell’s Palsy:
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
Exam of Bell’s Palsy:
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
PT goals for Bell’s Palsy:
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
Bulbar Palsy (bulbar paralysis):
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
Etiology of Bulbar Palsy:
result of tumors, vascular or degenerative diseases of lower cranial nerve motor nuclei (ALS)
Examof Bulbar Palsy:
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
Pseudobulbar Palsy
Bilateral dysfunction of corticobulbar innervation of brainstem nuclei
A central UMN lesion analogous to corticospinal lesions disrupting function of anterior horn cells
Symptoms of Pseudobulbar Palsy:
Produces similar symptoms of bulbar palsy
Examine for hyperactive reflexes: increased jaw jerk and snout reflex ( tapping on lips produces pouting of lips)
Signs and Symptoms of AIDS:
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
Alcoholic Ataxia:
A loss of coordination in performing voluntary movements associated with peripheral neuritis as a result of alcoholism
Signs and Symptoms of Alcoholic Ataxia:
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
Exam for Alcoholic Ataxia:
Romberg sign finger to nose test gait assessment (tandem gait) sensory testing DTR MMT to rule out weakness
Patient Management for Alcoholic Ataxia:
improve balance and postural reactions against external stimuli and gravitational
increases postural stabilization following joint stabilization
developing UE function
develop independent functional gait
Neocerebellar Lesions (Posterior):
Ipsilateral ataxia, Ipsilateral hypotonia & hyporeflexia, Dysmetria, Adiadochkinesia, movement decomposition, asthenia, intention tremors, rebound phenomenon, ataxic gait, staccato voice
Paleocerebellar Lesions (Anterior):
Disturbances in extensor tone (b/c this lobe receives the Spinocerebellar tracts – which when lost result in an ↑ in extensor tone.
Archicerebellar Lesions (Flocculonodular):
Uncoordinated trunk movements – ataxia. Balance deficits d/t loss of vestibular input from vestibular nuclei, cuneocerebellar tract, and rostral cerebellar tract
PT/OT for cerebellar dysfunction:
Added weight to help decrease tremor; but performance declines due to the added weight
Strengthening (help with deconditioning, weakness, or spasticity)
Speech for cerebellar dysfunction:
Swallowing exercises , dietary modification
Feeding by percutaneous endoscopic gastrostomy (PEG) tube
In advanced cases: feeding via PEG tube can reduce risk of aspiration
Cerebellar Dysfunction signs:
hypotonicity asthenia ataxia Dysmetria, Gait Disturbance, Movement Decomposition Dysdiadochokinesia, Speech, Eye Movement
Myasthenia Gravis:
A neuromuscular junction disorder characterized by progressive muscular weakness and fatigability on exertion
Etiology of Myasthenia gravis:
autoimmune antibody-mediated attack on acetylcholine receptors at neuromuscular junction
Characteristics of Myasthenia Gravis:
Muscular strength worse with continuing contraction, improved with rest
4 types of Myasthenia Gravis:
Ocular myasthenia
Mild generalized myasthenia
Severe generalized myasthenia
crisis
Generalized myasthenia
usually involves bulbar (extraocular, facial and muscles of mastication) and proximal limb girdle muscles
may progress from mild to severe within 18 month
Myasthenic crisis
myasthenia gravis with respiratory failure; treat as medical emergency
Myasthenia Gravis exam:
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
Which muscles are more involved in myasthenia gravis?
proximal more involved than distal, fatigability, repeated muscle use results in rapid weakness
Signs and Symptoms of Brian Tumor:
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
Grade I Tumor:
The tissue is benign. The cells look nearly like normal brain cells, and they grow slowly.
Grade II Tumor:
The tissue is malignant. The cells look less like normal cells than do the cells in a Grade I tumor
Grade III Tumor:
The malignant tissue has cells that look very different from normal cells. The abnormal cells are actively growing
Grade IV Tumor:
The malignant tissue has cells that look most abnormal and tend to grow quickly
Astrocytoma:
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
Meningioma:
The tumor arises in the meninges. It can be grade I, II, or III. It’s usually benign (grade I) and grows slowly
Oligodendroglia
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
Signs and Symptoms of Abscess:
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
Abscess Exam:
ataxia, papilledema general or focal seizures drowsiness hemiparesis slurred speech
