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enough to give the impression of a cerebellar stroke A suck re ex and grasp re exes of the hands and feet are variably present; plantar re exes are sometimes extensor Last, there may be sphincteric incontinence, often without the patient s awareness Occult hydrocephalus due to tumor growth is discussed in Chap 31 Clinical Picture of Acute Hydrocephalus Surprisingly little has been written about this syndrome despite its frequency in clinical practice It is seen most often following subarachnoid hemorrhage from a ruptured aneurysm, less often with bleeding from an arteriovenous malformation or from deep hemispheral hemorrhage that dissects into the ventricles; it may also occur as the result of obstruction of the CSF pathways in the fourth ventricle by a tumor or cerebellar-brainstem hemorrhage or within the basal cisterns by neoplastic in ltration of the meninges, although this last process tends to evolve more subacutely The patient complains of a headache of varying severity and often of visual obscuration, may vomit, and then becomes drowsy or stuporous over a period of minutes or hours Bilateral Babinski signs are the rule, and in the advanced stages, which are associated with coma, there is increased tone in the lower limbs and extensor posturing Early in the process, the pupils are normal in size and the eyes may rove horizontally; as the ventricles continue to enlarge, the pupils become miotic, the eyes then cease roving and assume an orthotopic position, or there may be bilateral abducens palsies and limitation of upward gaze The speed with which hydrocephalus develops determines whether there is accompanying papilledema If this condition is left untreated, the pupils eventually dilate symmetrically, the eyes no longer respond to oculocephalic maneuvers, and the limbs become accid Rarely, there is an unanticipated cardiac arrest, even at an early stage of evolution of the hydrocephalus; this complication is seen particularly in children and may be presaged by brain compression at the level of the perimesencephalic cisterns, detectable by imaging studies Treatment is by drainage of CSF, usually effected by a ventricular catheter or, if there is undoubted communication between all the CSF compartments, by lumbar puncture The latter may pose some risk if spinal uid is withdrawn rapidly, thereby creating a pressure gradient between the cerebral and spinal regions Neuropathologic Effects of Tension Hydrocephalus Ventricular expansion tends to be maximal in the frontal horns, explaining the hydrocephalic impairment of frontal lobe functions and of basal ganglionic frontal motor activity in all forms of hydrocephalus The central white matter yields to pressure, while the cortical gray matter, thalami, basal ganglia, and brainstem structures remain relatively unaffected There is an increase in the content of interstitial uid in the tissue adjacent to the lateral ventricles, readily detected by magnetic resonance imaging (MRI) (Fig 30-2) Myelinated bers and axons are injured, but not to the extent that one might expect from the degree of compression; minor degrees of astrocytic gliosis and loss of oligodendrocytes in the affected tissue are present to a decreasing extent away from the ventricles and represent a hydrocephalic atrophy of the brain The ventricles are characteristically denuded of ependyma and the choroid plexuses are attened and brotic The lumens of cerebral capillaries in biopsy preparations are said to be narrowed a nding that is dif cult to evaluate
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Normal-Pressure Hydrocephalus (See also
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pages 105 to 106) In nonprogressive meningeal and ependymal diseases, hydrocephalus may develop and reach a stable stage It is said to be compensated, in the sense that formation of CSF equilibrates with absorption The formation of CSF diminishes slightly, perhaps because of compression of the choroid plexuses; absorption increases in proportion to CSF pressure Once equilibrium is attained, the ICP gradually falls, though it still maintains a slightly higher gradient from ventricle to basal cistern to cerebral subarachnoid space A stage is reached where the CSF pressure reaches a high normal level of 150 to 200 mmH2O while the patient still manifests the cerebral effects of the hydrocephalic state The name given to this condition by Hakim, Adams and Fisher was normal-pressure hydrocephalus (NPH) A triad of clinical ndings is characteristic of NPH a slowly progressive gait disorder is usually the earliest feature, followed by impairment of mental function, and sphincteric incontinence Grasp re exes in the feet and falling attacks may also occur but there are no Babinski signs Headaches are infrequently a complaint, and there is no papilledema The gait disturbance may be of several different types, as discussed in Chap 7; some of them are dif cult to classify, but certain features predominate Most often it takes the form of unsteadiness and impairment of balance, with the greatest dif culty being encountered on stairs and curbs (Fisher) Weakness and tiredness of the legs are also frequent complaints, although examination discloses no paresis or ataxia The gait in NPH may convey an impression of Parkinson disease, with short steps and stooped, forward-leaning posture, but there is no rigidity, slowness of alternating movement, or tremor Other patients present with unexplained falls, often helplessly backward, but on casual inspection the gait may betray no abnormality at all When the condition remains untreated, the steps become shorter, with frequent shuf ing and falls; eventually standing and sitting and even turning over in bed become impossible Fisher refers to this advanced state as hydrocephalic astasia-abasia The mental changes in the cases we have encountered have been, broadly speaking, frontal in character and embody mainly apathy, dullness in thinking and actions, and slight inattention Memory trouble is usually a component of the overall problem and has been predominant in some cases, for which reason the diagnosis of Alzheimer disease has been made There is usually a degree of affective indifference but the patient reports little in the way of emotionality The extensive study of 63 patients by De Mol largely corroborated these impressions but also found dif culties in verbal, graphical, and calculation skills with which we have not been impressed It is notable that his patients with verbal dif culties did not improve with shunting, suggesting to us that they had a degenerative dementia Unfortunately, beyond the above-noted defects that are elicitable by routine testing, we have not found neuropsychologic tests of great value in the diagnosis of NPH Urinary symptoms appear relatively late in the illness Initially, they consist of urgency and frequency Later, the urgency is associated with incontinence, and ultimately there is frontal lobe incontinence, in which the patient is indifferent to his lapses of continence This syndrome of NPH may follow subarachnoid hemorrhage from ruptured aneurysm or head trauma, a resolved acute meningitis or a chronic meningitis (tubercular, syphilitic, or other), Paget
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