J. Richard Baringer

Herpes Simplex Infections of the Nervous System

Dramatic progress has been made recently in diagnosing and treating herpes simplex virus encephalitis (HSVE). Advances in imaging technology have greatly enhanced our ability to diagnose the illness noninvasively. Acyclovir is of proven efficacy and is generally well-tolerated. The major clinical management problem is that the pathologic process in the brain is usually well-advanced before the patient presents, and the symptoms, particularly in newborns or infants, are often initially nonspecific. This, plus a too frequent failure to recognize the nature and seriousness of the process, results in further delay in diagnosis and treatment. Physicians need to develop an increased awareness of the early signs and symptoms of the presentation of HSVE, and of the imperative for early treatment.

HERPES SIMPLEX VIRUS INFECTIONS OF THE NERVOUS SYSTEM

Herpes simplex virus is one of the group of herpes viruses responsible for a variety of human infections.1,2 These large enveloped DNA viruses, together comprising herpes simplex virus types I and II, cytomegalovirus, varicella zoster virus, and Epstein-Barr virus, are unique in that they all have the capability for persisting in humans for many years, though the sites and manner in which they persist appear to differ. Herpes simplex virus and varicella-zoster virus share the ability to produce segmental cutaneous disease which, in the case of herpes simplex, is probably related to its demonstrated potential to reside in sensory ganglia for many years. The same may be true for varicella zoster virus; direct proof of this is now emerging. Both herpes simplex virus and Epstein-Barr virus are suspected causes of human tumors, though the evidence for the latter is much more convincing. EB virus was first isolated from tumor tissues of patients with Burkitt’s lymphoma in Africa and has since been strongly implicated by DNA reassociation studies in nasopharyngeal tumors. Though a role for herpes simplex virus infection has been suspected on the basis of serologic evidence in human cervical cancer, a direct association between the virus and cervical cancer is still lacking.

Management Issues in Asymptomatic Carotid Stenosis

In the absence of symptoms, management is not clear-cut; indeed, are symptoms truly absent or merely unacknowledged? The workup must carefully balance risks associated with carotid endarterectomy against risks of nonsurgical treatment. Psychosocial factors are an important part of the balance; some patients prefer to live with the risk of stroke from essentially untreated disease.

Porphyrin-Laser Photodynamic Induction of Focal Brain Necrosis

Abstract. A noninvasive photodynamic method has been developed to produce focal brain necrosis using porphyrin activated in vivo with laser light. After peripheral injection of the photosensitive porphyrin derivative, Photofrin I, mice were irradiated on the posterior lateral aspect of the head through the intact depilated scalp with 632 nm argon-dye laser light. Animals were studied at one, two and seven days after irradiation. Blood-brain barrier damage was detected by the intravenous injection of Evans blue, horseradish peroxidase and heterologous immunoglobulins. At one and two days after irradiation, the lesions were characterized by extravasation of immunoglobulin and Evans blue, and by edema, ischemia and infiltration by monocytes. On the seventh day after irradiation, the lesion was smaller than it had been two days after irradiation, and had reactive changes at its edges and coagulative necrosis at its center. Extravasation of Evans blue and immunoglobulin was markedly reduced by the seventh day after irradiation, but uptake of horseradish peroxidase by macrophages located at the periphery of the lesion was evident.

Selecting treatment in patients with epilepsy

With improved understanding of epileptic syndromes during the past decade, the number of antiepilepsy medications has increased. Successful treatment starts with valaccurate diagnosis, because antiseizure drugs are fairly specific for particular syndromes and because surgery in some cases is superior to medical therapy.

CADASIL with Multiorgan Involvement: a Complete Autopsy Examination Report.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary disease of small blood vessels caused by mutations in the Notch3 gene. Tournier-Lasserve and Bousser described an autosomal dominant syndrome characterized mainly by recurrent strokes and neuroimaging evidence of leukoencephalopathy, studying 45 members of a single family clinically and with magnetic resonance imaging (MRI;) they were then the first to report the pathologic findings in one of the affected subjects, noting myelin loss and pallor sparing the U-fibers. Histopathological features of degeneration of the medial smooth muscle cells (SMCs) accompanied by deposition of periodic acid Schiff (PAS)-positive, electron dense granular osmiophilic material (GOM) in the small arteries and arterioles have been predominantly reported in autopsied brains and skin biopsies. Skin involvement in CADASIL is well known and a documented means of making the diagnosis other than genetic testing. Despite this, extra-neurologic organ involvement in CADASIL has rarely been documented.

Current Therapy of Multiple Sclerosis

The list of medications for both immune modulation and symptomatic relief continues to grow. Ideally, however, drug therapy should be part of a multidisciplinary approach that also includes such elements as patient education and physical therapy.

Defusing Status Epilepticus

The risk of brain neuron death supersedes that of physical harm due to muscle spasms. In fact, immediate induction of neuromuscular paralysis impedes monitoring of anticonvulsant therapy, which can be empiric but should follow a predetermined, sequential protocol so that seizures can be terminated quickly.The risk of brain neuron death supersedes that of physical harm due to muscle spasms. In fact, immediate induction of neuromuscular paralysis impedes monitoring of anticonvulsant therapy, which can be empiric but should follow a predetermined, sequential protocol so that seizures can be terminated quickly.