Nuclear Brain Stem Syndromes

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Trauma, ischemic injury, and tumors may affect the trigeminal system within the brain stem. These syndromes are characterized by sensory paresthesias, numbness, or pain in the distribution of the V1 to V3, along with combinations of cranial nerve palsies and distinct sensory and cerebellar system signs. Reflecting the lateral circumferential

TABLE 10-3 -- SELECTED ETIOLOGIES ASSOCIATED WITH TRIGEMINAL NERVE DISORDERS

Etiological Category

Selected Specific Etiologies

Chapter

STRUCTURAL DISORDERS

Developmental

Brain stem vascular loop, syringobulbia

28

Degenerative and compressive

Paget's disease

29

HEREDITARY AND DEGENERATIVE DISORDERS

Chromosomal abnormalities and neurocutaneous disorders

Hereditary sensorimotor neuropathy 1 Neurofibromatosis ( schwannoma)

32

Degenerative motor, sensory, and autonomic disorders

Amyotrophic lateral sclerosis

36

ACQUIRED METABOLIC AND NUTRITIONAL DISORDERS

Endogenous metabolic disorders

Diabetes

38

Exogenous disorders: Toxins and illicit drugs

Trichlorocthylene, tnehloroacetie acid

39

Nutritional deficiencies., and syndromes associated with alcoholism

Thiamine, folate, Bl2 , pyndoxine, pantothenie acid, vitamin A deficieney

40

INFECTIOUS DISORDERS

Viral infections

Herpes zoster, unknown

41

Non-viral infections

Bacterial, tuberculous meningitis, brain abscess, Gradenigos syndrome,leprosy, cavernous sinus thrombosis

43

HIV and AIDS

Opportunistic infections abscesses, herpes zoster

44

NEUROVASCULAR DISORDERS

Stroke, hemorrhage, aneurysm

45

NEOPLASTIC DISORDERS

Primary neurological tumors

Glial tumors, meningioma, schwannoma

46

Metastatic neoplasms and paraneoplastic syndromes

Lung, breast, Iymphoma, carcinomatous meningitis

47

DEMYELINATING DISORDERS

Demyelinating disorders of the central nervous system

Multiple seleOrosis, acute demyelinating encephalomyelitis

48

Demyelinating disorders of the peripheral nervous system

Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy

49

AUTOIMMUNE AND INFLAMMATORY DISORDERS

Tolosa-Hunt syndrome, sarcoidosis, lupus, orbital pseudotumor

50

TRAUMATIC DISORDERS

Carotid cavernous fistula, cavernous sinus thrombosis, maxillary/ mandibular injury

51

EPILEPSY

Focal seizures

52

HEADACHE AND FACIAL PAIN

Raeders neuralgia, cluster headache

53

DRUG-INDUCED AND IATROGENIC NEUROLOGICAL DISORDERS

Orbital, facial, dental surgery

55

arterial supply to the lateral pons, ischemic lesions of the pontine tegmentum are often associated with dissociation of sensory modalities such that pain and temperature perception are dramatically diminished, whereas midline fiber tracts carrying light touch and deep pressure are spared. Pain similar to that of trigeminal neuralgia is rare. The lateral medullary or Wallenberg's syndrome 21 typically results from ischemic infarction of either the vertebral or posterior inferior cerebellar arteries, which provide vascular supply to the lateral medulla (.Fig 10-5 ). Sensory loss may affect the entire ipsilateral face. Sensory loss results from damage to the spinal trigeminal tract, its nucleus, and rostral trigeminothalamic projections. Interestingly, some patients with Wallenberg's syndrome report facial pain or headache before neurological deficit. y

Persistent ipsilateral pain may be present in up to 50 percent of patients with a lateral medullary syndrome y typically in V1 or V2 distribution, which in some persists for months to years after the acute insult. The pattern of facial analgesia in patients with lateral medullary syndrome typically adheres to the cutaneous distribution of V1 to V3, although an onion-skin or radicular pattern of sensory loss has been described in which lesions affecting more rostral portions of the trigeminal sensory nuclei result in sensory loss in the nose and lips, whereas rostral and caudal lesions yield sensory loss in the cheeks and forehead. Associated neurological symptoms with Wallenberg's syndrome include ipsilateral Horner's syndrome, ataxia, and difficulty swallowing, with pain and temperature loss on the contralateral body (due to damage to the ascending spinothalamic tract). Lesions affecting the spinothalamic and spinal trigeminal tracts in the lateral medulla typically result in this crossed pattern of hemifacial and hemibody sensory loss (ipsilateral facial numbness with contralateral arm and leg numbness). Lesions involving more medial medullary regions result in unilateral facial and bodily sensory deficits contralateral to the lesion. y Medial medullary lesions presumably injure the crossed ventral trigeminothalamic tract.

Other pathological processes within the brain stem can produce trigeminal dysfunction. Tumors, hemorrhage (hypertensive, ruptured arteriovenous malformation), infarctions, demyelinating disease such as multiple sclerosis, infections such as brain stem abscesses and brain stem encephalitis, and inflammatory conditions such as tuberculosis or sarcoidosis affecting the lateral pons or midbrain may result in ipsilateral or contralateral facial sensory loss, respectively, as well as severe paroxysmal hemifacial pain. Facial weakness, muscle atrophy, difficulty chewing, and diminished jaw jerk reflex may be identified in amyotrophic lateral sclerosis as well as other motor neuron disorders damaging the motor trigeminal nuclei. Traumatic or congenital syringobulbia can affect the sensory and motor portions of the trigeminal system within the midbrain, pons, or medulla.

Figure 10-5 Left-sided trigeminal nerve involvement from sarcoid involving the skull base and meninges. Weakness of the pterygoids and masseters manifested as ipsilateral (leftward) jaw deviation and weakness of jaw opening.

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