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The infectious etiology of sarcoidosis has never been established, but the disease may suitably be considered at this point because of its close resemblance pathologically and clinically to tuberculosis and other granulomatous infections Indeed, one still credible theory of causation considers sarcoidosis to be a modi ed form or product of the tubercle bacillus This has not been proved, and the same can be said for various other infectious and noninfectious etiologies that from time to time have been proposed as the underlying cause Current opinion favors the idea that sarcoidosis represents an exaggerated cellular immune response to a limited class of antigens or autoantigens (Crystal) The essential lesion in sarcoidosis consists of focal collections of epithelioid cells surrounded by a rim of lymphocytes; frequently there are giant cells, but caseation is lacking The sarcoid tubercles may be found in all organs and tissues including the peripheral and CNS, but the most frequently involved are the mediastinal and peripheral lymph nodes, lungs, liver, skin, phalangeal bones, eyes, and parotid glands Sarcoidosis is accompanied by nervous system involvement (neurosarcoidosis) in approximately 5 percent of cases according to the worldwide surveys of Delaney and of Siltzbach and colleagues It may take any one of several forms As indicated in Chaps 13, 46 and 47, isolated sarcoid granulomas may involve peripheral or cranial nerves, giving rise to a subacute or chronic neuropathy or plexopathy of asymmetrical type (Jefferson) Polyneuropathy may occur but is rare; Zuniga and colleagues have summarized our own experience Of the cranial nerves, the facial is the most frequently involved, either as part of the uveoparotid syndrome (Heerfordt syndrome) or independently The facial palsy may be unilateral or bilateral; if the latter, the nerves may be affected simultaneously or in succession The occurrence of hyperacusis indicates that the lesion is central to the stylomastoid foramen Blindness may follow basal in ltration that encompasses the optic nerves (Fig 32-4) CNS sarcoidosis is said to be infrequent, but we encounter one or more cases yearly Several syndromes are known that are due to localized involvement of the meninges, brain, and spinal cord (Table 32-5) In Scadding s series of 275 patients, only 3 developed CNS lesions; in other large series, the incidence of CNS involvement was greater, but most are in the range of 5 to 10 percent (10 of 145 patients studied by Mayock et al; 14 of 285, by Chen and McLeod; and 33 of 649, by Stern et al) Delaney, in his review of the literature, found the neurologic involvement in sar-.

Table 32-5 Nervous system manifestations of sarcoidosis Aseptic meningitis: chronic or relapsing, with or without headache Pachymeningitis: hydrocephalus Brain Focal tumor-like mass: seizures, hemiparesis Cortical and subcortical in ltration; amnestic-dementing syndrome, encephalopathy, headache Hypothalamic-basilar in ltration: diabetes insipidus, abulia Spinal cord and roots Granulomatous meningomyelitis, subacute or chronic Cauda equina syndrome Peripheral nervous system Lumbar or brachial plexopathy Sensory-predominant polyneuropathy Mononeuropathy Mononeuritis multiplex Cranial neuropathy Visual loss Papillitis Facial palsy, unilateral, bilateral, or sequential Hearing loss, vertigo Facial sensory loss or neuralgia

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coidosis to be equally divided between the peripheral and central nervous systems There is also a well-described myopathy associated with sarcoidosis; it is discussed below and also considered in Chap 49; the neuropathy of sarcoidosis is discussed in Chap 46 In the CNS, sarcoidosis takes the form of a granulomatous in ltration of the meninges and underlying parenchyma, most frequent at the base of the brain (Fig 32-4) The process is subacute or chronic in nature, mimicking other granulomatous lesions and neoplasms One particular syndrome that has been associated with sarcoid consists of a circumscribed lesion of the stalk of the pituitary gland, optic chiasm, and hypothalamus, causing visual disturbances, polydipsia, polyuria, or somnolence Hydrocephalus, seizures, cranial nerve palsies, and corticospinal and cerebellar signs are other occasional manifestations Rarely sarcoid can be a cause of a chronic recurrent meningitis, or severe, steroid-responsive headache Granulomas may present as a mass or as one or more focal in ltrating cortical and subcortical lesions that tends to follow the course of super cial cortical veins Focal cerebral signs, including seizures, due presumably to large focal deposits of sarcoid in the brain, are observed Among the focal syndromes reported have been an amnestic or dementing condition from in ltration of the medial temporal lobes and psychotic and related behavioral aberrations The spinal meninges and spinal cord may be in ltrated, usually independently of brain involvement, imparting a picture of adhesive arachnoiditis or an in ammatory myelopathy There is more prominent focal contrast enhancement and T2 signal abnormality on MRI than is usual for a demyelinating disease Characteristic of the spinal lesion is enhancement on the surface of the cord and a degree of expansion at the level of the myelitic lesion (page 1060) We have had experience with several such cases in which the only evidence of sarcoid was a lesion in the thoracic cord; in the absence of systemic manifestations of sarcoid Biopsy of the spinal cord lesion, a risky procedure, was necessary for diagnosis in 2 cases.

Now suppose that EB is made positive, starting at small voltages and gradually increasing If this forward bias is less than the forward breakover voltage, no current will flow But as the base voltage EB reaches breakover, the E-B junction will start to conduct The base-collector (B-C) junction will remain reverse-biased as long as EB is less than the supply voltage (in this case 12 V) In practical transistor circuits, it is common for EB to be set at a fraction of the supply voltage Despite the reverse bias of the B-C junction, the emitter-collector current, called collector current and denoted IC, will flow once the E-B junction conducts In a real transistor (Fig 22-3B), the meter reading will jump when the forward breakover voltage of the E-B junction is reached Then even a small rise in EB, attended by a rise in IB, will cause a big increase in IC This is shown graphically in Fig 22-4

Figure 32-4 Cerebral sarcoid Gadolinium-enhanced MRI of the brain Top panel: Sarcoid lesions coat the base of the brain and cerebellum and surround the pituitary stalk The patient had pulmonary sarcoid, marked abulia, and panhypopituitarism Bottom panel: Sarcoid in ltration of the basal pachymeninges and both optic nerves causing blindness Visual acuity returned almost to normal after 2 weeks of corticosteroid administration

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