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It should be stated at the outset that syncope is an uncommon manifestation of cerebrovascular disease; cases that do occur are usually associated with multiple occlusions of the large arteries in the neck The best examples are found in patients with the aortic-arch syndrome (Takayasu pulseless disease, page 732), in which the brachiocephalic, common carotid, and vertebral arteries have become narrowed Physical activity may then critically reduce blood ow to the upper part of the brainstem, causing abrupt loss of consciousness Stenosis or occlusion of vertebral arteries and the subclavian steal syndrome are other examples (page 678) Fainting is said also to occur occasionally in patients with congenital anomalies of the upper cervical spine (Klippel-Feil syndrome) or cervical spondylosis, in which the vertebral circulation is compromised Head turning may then cause vertigo, nausea and vomiting, visual scotomas, and nally unconsciousness Syncope does not occur with ischemic attacks that are con ned to the territory of the internal carotid artery Nor, in the authors experience, do pure syncopal attacks occur with vertebrobasilar ischemia (see further on) Cerebral Hemorrhage and Syncope The onset of a subarachnoid hemorrhage may be signaled by a syncopal episode, often with transient apnea Because the bleeding is arterial, there is a momentary cessation of cerebral circulation as intracranial pressure and blood pressure approach one another Unless there has been vomiting, a complaint of headache immediately preceding the syncope, or the discovery of hypertension or stiff neck when the patient awakens, the diagnosis may not be suspected until a CT scan or lumbar puncture is performed

Anxiety Attacks and the Hyperventilation Syndrome These are probably the most important diagnostic considerations in unexplained faintness without syncope The light-headedness of anxiety and hyperventilation are frequently described as a feeling of faintness, but a loss of consciousness does not follow (see Linzer et al) Such symptoms are not accompanied by facial pallor or relieved by recumbency The diagnosis is made on the basis of the associated symptoms, the absence of laboratory and tilt-table abnormalities, and the nding that part of the attack can be reproduced by having the patient hyperventilate The symptoms produced in this way mimic the persistent or episodic dizziness that accompanies anxiety and panic states (Chap 15) When anxiety attacks are combined with a Valsalva effect or prolonged standing, fainting may occur The relationship of anxiety-panic to the previously described postural orthostatic tachycardia syndrome is uncertain Hypoglycemia In nondiabetics, hypoglycemia may be an obscure cause of episodic weakness and very rarely of syncope With progressive lowering of blood glucose, the clinical picture is one of hunger, trembling, ushed facies, sweating, confusion, and nally,

Imaging techniques computed tomography (CT), magnetic resonance imaging (MRI), and ultrasound enable one to measure

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muscle volume and to recognize qualitative changes in muscle structure (see review of deVisser and Reimers) Such methods are nding increasing clinical and research use in the diagnosis of disorders of muscle and in gauging the effects of treatment CT scans of dystrophic muscle show foci of decreased attenuation, representing masses of fat cells The fatty masses spread gradually from multiple foci and eventually replace muscle bers The original shape of the muscle is retained; indeed, an enlarged weak muscle containing mostly fat con rms the clinical impression of pseudohypertrophy In denervative atrophy, the muscles are obviously small and contain multiple punctate areas of decreased attenuation, which represent interstitial fat Eventually, large portions of chronically denervated muscle may be replaced by fat Blood, blood products, and calcium deposits are expressed by increased attenuation in CT This may be helpful in the diagnosis of muscle trauma, myositis ossi cans, and polymyositis In MR images, fat and bone marrow have a high signal intensity, while fascia, ligaments, and cortical bone lack signal intensity In T1-weighted images, normal muscle has a low signal and dystrophic muscle, a slightly increased signal; in T2-weighted images, dystrophic muscle has a slightly enhanced signal Given its sensitivity to these dystrophic changes in muscle, MRI is particularly effective in determining the distribution of muscle involvement in a dystrophy Transverse MR sections, for example, can help distinguish the topographic patterns of such disorders as the proximally predominant Becker dystrophy and the distally predominant Miyoshi myopathy or subtle subtypes of Emery-Dreifuss dystrophy (Mercuri) Spectroscopic MRI in metabolically determined myopathies has the capacity to quantitate levels of selected biochemical constituents of muscle, including intracellular pH and levels of metabolic intermediates such as phosphocreatine This is particularly effective in demonstrating subnormal generation of intracellular acidosis after a limb is exercised in disorders of glycogenolysis and of glycolysis Some individuals with mitochondrial disease of muscle will demonstrate rapid depletion of energy supplies and profound delays in recovery that can be quanti ed and used as an endpoint for treatments New magnetic resonance techniques are also being developed that allow the imaging of nerves This may be an aid in traumatic nerve injury and in demonstrating neuromas, hypertrophy or atrophy of a nerve trunk, as well as neural tumors.

Muscle biopsy can be of great diagnostic value, but both surgical and microscopic techniques must be exacting The muscle chosen for study should be accessible; there should be evidence that it has been affected but not totally destroyed by the disease in question; and it should not have been the site of a recent injection or EMG study, since the trauma of the needles produces focal necrotizing and in ammatory lesions Muscle biopsy is helpful in distinguishing the following basic disorders in patients with neuromuscular disease 4

1 Denervation atrophy Reduction in the size of muscle bers with an accompanying enlargement of intact motor units (due to collateral reinnervation) and degenerative changes in some bers are the main changes of denervation atrophy 5

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TABLE 6-6