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ronal death is likely to be more complex than is currently envisioned However, the extent of neural tissue dysfunction is not dictated solely by the activation of these mechanisms in neurons It is now clear that highly toxic in uences are exerted on oligodendroglial cells in white matter during ischemia Moreover, the injury to both neurons and oligodendroglial cells is augmented in brain tissues by an in ammatory response to the initial injury, activating endothelial cells to express cell adhesion molecules that can attract additional in ammatory cells and upregulating levels of in ammatory proteases (eg, metalloproteases) and cytokines (eg interleukins and chemokines) These events are summarized in the review by Lo and coworkers It is evident that these events are highly complex, invoking multiple parallel molecular phenomena The salient feature of these molecular pathways is that they provide points for potential therapeutic interventions As one example, it is clear that as ATP production fails and energy gradients are depleted, there is signi cant accumulation of lactic acid in cerebral tissue, and all the biochemical changes consequent to the cellular acidosis occur These may also be of importance in determining the extent of cell damage (see reviews of Raichle and of Plum) Myers and Yamaguchi showed that monkeys infused with glucose before the induction of cardiac arrest suffered more brain damage than did either fasted or salineinfused animals They suggested that the high cerebral glucose level under anaerobic conditions led to increased glycolysis during the ischemic episode and that the accumulated lactate was neurotoxic On the basis of such observations, Plum has suggested that scrupulous control of the blood glucose might reduce the risk of cerebral infarction in diabetic and other stroke-prone patients and during conditions of potential hyperglycemia Clinical implementation of this idea is dif cult and its advantages remain to be established Regarding anoxic damage of the brain, Ames and Nesbett have studied the rabbit retina in an immersion chamber in which O2 and various substrates could be altered directly rather than through the vasculature They found that cells could withstand complete absence of O2 for 20 min After 30 min of anoxia, there was irreversible damage, re ected by an inability of the tissue to utilize glucose and to synthesize protein Hypoglycemia further reduced the tolerance to hypoxia, whereas the tolerance could be prolonged by reducing the energy requirements of cells (increasing magnesium in the medium) Ames postulated that the long period of tolerance of retinal neurons to complete anoxia in vitro, in comparison to that in vivo, is related to what he called the no-re ow phenomenon (swelling of capillary endothelial cells, which prevents the restoration of circulation), as mentioned earlier Body temperature is yet another important factor in determining the extent of infarction A reduction of even 2 to 3 C (36 to 54 F) reduces the metabolic requirements of neurons and increases their tolerance to hypoxia by 25 to 30 percent These biochemical, cellular, and CBF ndings enable one to conceptualize maneuvers for restoring blood ow within the marginally hypoperfused zone and salvaging brain tissue, particularly since under conditions of partial ischemia, cerebral tissue may survive for periods of 5 to 6 h or even longer.

suf cient uniformity to justify the assignment of a typical syndrome to each of the major arteries and their branches The following descriptions apply particularly to the clinical effects of ischemia and infarction due to embolism and thrombosis The identi cation by careful examination of highly speci c neurovascular syndromes is one of cardinal skills of the clinical neurologist Although hemorrhage within a speci c vascular territory may give rise to many of the same effects, the total clinical picture is different because it usually involves regions supplied by more than one artery and, by its deep extension and pressure effects, causes secondary features of headache, vomiting, and hypertension as well as a series of falsely localizing signs, as described in Chaps 17 and 31

Table 24-1

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or more often by an opportunistic CMV infection in a patient with AIDS Diagnosis This is both aided and at times confused by serologic testing (see Chap 32) The enzyme-linked immunosorbent assay (ELISA) is not altogether satisfactory because it frequently yields false-positive and, occasionally, false-negative results Western blot testing is more speci c Knowledge that the patient has lived in or visited an endemic area is useful but far more important is evidence of a tick bite followed by the characteristic rash or a wellde ned history of nonneurologic manifestations of Lyme disease (cardiac, arthritic) Indeed, one should be cautious in making this diagnosis unless a primary Lyme infectious syndrome had been present Bifacial palsy in any of these clinical contexts also favors the diagnosis Treatment Treatment of the neuropathic disease is with intravenous antibiotics, preferably ceftriaxone 2 g daily for 1 month Corticosteroids have an uncertain role in the painful radicular syndromes but we have used them in low doses and they apparently relieved the pain Sjogren-Sicca Syndrome This is a chronic, slowly progressive autoimmune disease characterized by lymphocytic in ltration of the exocrine glands, particularly the parotid and lacrimal glands resulting in keratoconjunctivitis sicca and xerostomia (dry eyes and mouth) The latter features may be combined with arthritis or with a wide range of other abnormalities, notably lymphoma, vasculitis, renal tubular defects, and quite often by a predominantly sensory polyneuropathy (see review by Kaplan et al) In the series collected by Grant and colleagues, the neuropathy was the presenting problem in 87 percent of 54 patients with the sicca complex The sicca symptoms are usually mild and often reported only upon speci c inquiry A symmetrical sensory polyneuropathy or sensory ganglionopathy is the most common pattern Sensorimotor polyneuropathy, polyradiculoneuropathy, autonomic neuropathy, or mononeuropathy (most often of the trigeminal nerve, as described by Kaltrieder and Talal) are less common We have observed yet another neuropathic syndrome taking the form of an asymmetrical sensory loss, mostly of position sense and involving the upper limbs predominantly, in association with tonic pupils and trigeminal anesthesia The sensory polyneuropathy of the Sjogren syndrome more of an in ammatory ganglionitis or sensory neuronopathy (Grif n et al) is of particular interest to neurologists, since most cases will rst be seen by them More than 90 percent of the patients are older women The sensorimotor polyneuropathic syndrome begins with paresthesias of the feet and is usually mild in degree The main clinical features are a subacute and widespread sensory loss that may include the trunk and a profoundly diminished kinesthetic sense, giving rise to sensory ataxia of the limb and of gait Loss of pain and temperature sensation is variable; tendon re exes are abolished In time, many of these patients develop autonomic abnormalities such as bowel atony, urinary retention, loss of sweating, and pupillary changes There is usually little or no pain but there have been exceptions Diagnosis Sjogren syndrome should be suspected in an older woman with sensory neuropathy or neuronopathy, particularly if sicca symptoms are present The evaluation of suspected Sjogren disease is aided by the Schirmer or Rose Bengal tests (page 461), which can demonstrate a reduction of tearing Even without this con rmatory test, we have found it advisable to perform a biopsy of the lip (at the epithelial-mucosal juncture) to detect in ammatory.

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