Cranial and Peripheral Nerve Lesions
General Principles of Nerve Injury
Injury to single nerve (mononeuropathy): most commonly follows trauma. Toxic or metabolic disorders affect many nerves (mononeuropathy multiplex or symmetric polyneuropathy).
Pathophysiology
Three major types of injury. (1) nerve transection (neurotmesis); (2) axonal interruption with distal degeneration but preserved endoneurium (axonotmesis); (3) mild ischemic compressive injury resulting in conduction block at site of lesion but without axonal or endoneurial disruption, without degeneration of distal axons (neurapraxia).
Clinical Features
Motor nerves: flaccid paralysis, wasting of muscles innervated by affected nerve.
Sensory nerves: loss of sensation in distribution of nerve.
Partial injury may cause stabbing pain, pins-and-needles sensation (paresthesias), severe burning pain (causalgia).
Vasomotor disorders, “trophic disturbances” (changes in skin, mucous membranes, bones, nails) more common with injury of sensory or mixed nerves than motor. See also complex regional pain syndrome (reflex sympathetic dystrophy), Chapter 71.
Diagnosis
Distribution of motor and sensory abnormalities (described later in chapter).
Differentiation from spinal root lesions, where weakness, sensory loss segmental, not in nerve distribution.
EMG shows patterns of denervation and reinnervation. Nerve conduction studies ascertain site of injury.
Prognosis
Probability of regeneration lower for injuries near CNS or more severe axonal injury.
Treatment
Surgical repair (selected injuries); rehabilitation.
Cranial Neuropathies
Olfactory Nerve and Tract
Lesions of nerve: loss of sense of smell, taste. Injury to CNS connections: often no loss of smell or taste. Temporal lobe lesions, seizures: transient olfactory hallucinations.
Most common cause: head trauma. Usually permanent.
Optic Nerve and Tract
Manifestations: loss of vision, impaired pupillary light reflexes, abnormal size of pupil (Table 69.1).
Causes: direct trauma, toxins, systemic diseases (e.g., diabetes mellitus, giant cell arteritis), demyelinating; heritable diseases, local conditions (e.g., glaucoma, retinal vein thrombosis), infiltration or compression of nerve, increased intracranial pressure. See also Chapter 7.
Optic neuritis: impaired visual acuity; caused by inflammatory, degenerative, demyelinating, toxic disorders.
Bedside Examination
Visual fields by confrontation. Hemianopia, quadrantanopia: retrochiasmatic lesion.
Visual acuity: optic nerve dysfunction. Also see reduced perception of color saturation (test with small red object).
Blind spot enlargement (test by confrontation): papilledema (e.g., increased intracranial pressure).
Pupil size. Contracted: pontine lesion, sympathetic dysfunction, opiate overdose. Dilated: parasympathetic dysfunction (including lesions in oculomotor nerve).
Pupil reactivity. Failure of one pupil to constrict when light is shone into either eye: parasympathetic dysfunction (e.g., oculomotor nerve compression). Failure of one pupil to constrict when light is shone into the same eye, with intact constriction when light is shown into the other eye (relative afferent pupillary defect): optic nerve (e.g., optic neuritis); see also Chapter 7. Failure to dilate when room is darkened: sympathetic dysfunction (e.g., Horner’s syndrome).
Pain on eye movements: optic neuritis.
Convergence, accommodation: abnormal in neurosyphilis, compression of dorsal midbrain (Parinaud syndrome; see Chapter 58).
Oculomotor, Trochlear, Abducens Nerves
Manifestations: diplopia, deviated eye, impaired ocular movement. See also Chapter 7.
Causes: head trauma, tumors or aneurysms at skull base, brainstem stroke, venous sinus thrombosis (e.g., cavernous sinus thrombosis), neurosyphilis, neurosarcoidosis, MS, meningitis, encephalitis, diphtheria, diabetes mellitus, lead poisoning, botulism, Wernicke encephalitis, skull osteomyelitis,
spinal anesthesia, lumbar puncture, increased intracranial pressure.
Third nerve or nucleus: paralysis of medial rectus, superior rectus, inferior rectus, inferior oblique, levator palpebrae superior; paralysis of constrictor ciliary muscles. Ptosis, eye deviated outward; pupil dilated, no reaction to light or accommodation.
Fourth nerve or nucleus: paralysis of superior oblique muscle, impaired ability to turn eye down and in. Diplopia ameliorated by tilting head forward and toward normal eye.
Sixth nerve: paralysis of lateral rectus. Eye deviated inward. Diplopia in all gaze directions.
Sixth nerve nucleus: paralysis of lateral gaze to affected side; neither eye moves beyond midline. Convergence preserved.
Tolosa-Hunt syndrome: painful ophthalmoplegia with MRI evidence of intracavernous inflammation.
Table 69.1 Effects of Lesions of the Optic, Oculomotor, and Sympathetic Pathways on the Pupils | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
