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and Latov and coworkers have shown that the serum IgM fraction often displays antimyelin activity Typically, the monoclonal protein in the blood is present in a concentration less than 2 g/100 mL and there is no evidence of multiple myeloma or other malignant disease It should be emphasized that routine serum protein electrophoresis (SPEP) fails to detect the majority of these paraproteins; immunoelectrophoresis (IEP) or the more sophisticated immuno xation testing is required The bone marrow aspirate shows a normal or only mildly increased proportion of plasma cells, which are the ostensible source of the paraprotein, and the plasma cells are not morphologically atypical, as they are in myeloma Insofar as myeloma becomes manifest in fewer than one quarter of patients many years after the gammopathy has been recognized, the condition is now termed monoclonal gammopathy of undetermined signi cance (MGUS), although the older term, benign monoclonal gammopathy, is less cumbersome The importance of excess immunoglobulin can be appreciated by noting that some 6 percent of patients referred to the Mayo Clinic with chronic polyneuropathy of unknown cause and as many as 20 percent in our clinical material and in other series have proved to have a monoclonal paraproteinemia (of course, the majority of patients with a blood paraprotein do not develop neuropathy) Despite the fact that IgG is the most frequent paraprotein in adults, a polyneuropathy is associated somewhat more often with the IgM class Combining three large series of patients with neuropathy and monoclonal paraproteinemias (62 patients of Yeung et al, 65 patients of Gosselin et al, and 34 of our patients reported by Simovic et al), there were 96 with IgM, 50 with IgG, and 15 with IgA subclass paraproteins An identical but infrequent condition exists in which only the light chain component of an immunoglobulin is overproduced by the plasma cells and is found exclusively in the urine (similar to the Bence-Jones protein of multiple myeloma) Most affected patients have had a kappa light chain component although lambda light chain has special signi cance as discussed further on in relation to plasmacytoma and the POEMS syndrome In our experience and in that of others, the group with IgM paraprotein has more often displayed severe sensory ndings and a demyelinative type of EMG abnormality when compared with the IgG group However, with the exception of the special antimyelin-associated glycoprotein (MAG) syndrome (see later), we have not found the degrees of difference in clinical features and response to treatment between the immunoglobulin subclasses that has been reported by others (Simovic et al) Although more than a dozen speci c antibodies against myelin and other components of nerve have been identi ed among the paraproteins, the most important ones, present in 50 to 75 percent of patients with IgM-associated neuropathies, are the ones that react with a MAG, related glycolipids, or sulfatide components of myelin (referred to as SGPG and SPLPG) Deep sensory loss with gait imbalance, severe tremor, and a Romberg sign are typical ndings in the group with anti-MAG activity, while weakness and atrophy tend to appear later in the illness Other IgM antineural antibodies have a more tentative connection to polyneuropathy Polyclonal IgM antibodies against the GM1 antigen of myelin are linked with multifocal motor conduction block, described further on, but are sometimes found coincidentally in patients with anti-MAG protein It is reasonable to assume that IgG monoclonal gammopathies are also capable of causing chronic neuropathies, but the evidence is less compelling and based mainly on the frequency of their coincidence Indeed, it has been suggested that in many reported in-.

higher rates, but it is clear that the cognitive problems improve over time in the majority of patients The use of Doppler insonation of the middle cerebral arteries is being studied to detect transient signals called HITs (high-intensity transients) as a manifestation of small emboli during surgery but, as in cerebral arteriography, the clinical importance of these emboli is not known The special stroke problems relating to prosthetic heart valves mainly infective endocarditis causing embolic strokes and anticoagulant-related cerebral hemorrhage are described in appropriate sections of this chapter

This is the third most frequent cause of stroke Although more than a dozen causes of nontraumatic intracranial hemorrhage are listed in Table 34-9, primary or hypertensive ( spontaneous ) intracerebral hemorrhage, ruptured saccular aneurysm and vascular malformation, and hemorrhage associated with the use of anticoagulants or thrombolytic agents account for the majority Cerebrovascular amyloidosis and bleeding disorders account for a small number The small brainstem hemorrhages secondary to temporal lobe herniation and brainstem compression (Duret hemorrhages), hypertensive encephalopathy, and brain purpura might be included in this group, but they do not simulate a stroke

This is the mundane spontaneous brain hemorrhage It is due predominantly to chronic hypertension and degenerative changes in cerebral arteries In recent decades, with increased awareness of the need to control blood pressure, the proportion of hemorrhages attributable to causes other than hypertension has greatly increased; more than half such hemorrhages on our services now occur in Table 34-9 Causes of intracranial hemorrhage (including intracerebral, subarachnoid, ventricular, and subdural) 1 Primary (hypertensive) intracerebral hemorrhage 2 Ruptured saccular aneurysm 3 Ruptured AVM; less often, venous and dural vascular malformations 4 Cavernous angioma 5 Trauma including posttraumatic delayed apoplexy 6 Hemorrhagic disorders: leukemia, aplastic anemia, thrombocytopenic purpura, liver disease, complication of anticoagulant or thrombolytic therapy, hypo brinogenemia, hemophilia, Christmas disease, etc 7 Hemorrhage into primary and secondary brain tumors 8 Septic embolism, mycotic aneurysm 9 With hemorrhagic infarction, arterial or venous 10 With in ammatory and infectious disease of the arteries and veins 11 With arterial amyloidosis 12 Miscellaneous rare types: vasopressor drugs, cocaine, moyamoya, herpes simplex encephalitis, vertebral artery dissection, acute necrotizing hemorrhagic encephalitis (Hurst disease), tularemia, anthrax, etc

The following illustration shows some of the options that are available if we use the General Template Settings functionality To access this dialog box, click the button to the right of the blank Template Properties field

normotensive individuals, and the hemorrhages more often than previously arise in locations that are not typical for hypertension Nevertheless, the hypertensive cerebral hemorrhage serves as a paradigm for understanding and managing the cerebral hemorrhage In order of frequency, the most common sites of a cerebral hemorrhage are (1) the putamen and adjacent internal capsule (50 percent); (2) the central white matter of the temporal, parietal, or frontal lobes (lobar hemorrhages, not strictly associated with hypertension); (3) the thalamus; (4) a cerebellar hemisphere; and (5) the pons (see Weisberg et al) The vessel involved is usually a penetrating artery that originates from a larger trunk vessel About 2 percent of primary hemorrhages are multiple Rarely the bleeding is solely intraventricular, possibly from the choroid plexus The problem is one of bleeding that occurs within brain tissue; rupture of arteries lying in the subarachnoid space is practically unknown apart from aneurysms and some vascular malformations The extravasation of blood forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues (Fig 34-20) Adjacent brain tissue is distorted and compressed If the hemorrhage is large, midline structures are displaced to the opposite side and reticular activating and respiratory centers can be compromised, leading to coma and death in the manner described in Chap 17 Both the size and the location of the clot determine the degree of upper brainstem compression (Andrew et al) Rupture or seepage into the ventricular system may occur, and the CSF becomes bloody in these cases However, a hemorrhage of this type almost never ruptures through the cerebral cortex When the hemorrhage is small and located at a distance from the ventricles, the CSF may remain clear even on repeated examina-