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NEUROLOGIC DISEASES
 
 
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Aseptic Meningitis Multiple Sclerosis Acute Encephalitis Epilepsy
Arboviruses Cerebral Infarction Herpes Simplex Virus Cerebral Haemorrhage
Herpes Zoster Brain Tumours Poliomyelitis Spinal-Cord Tumours
Slow Virus Infections Guillain-Barre Syndrome Neurosyphilis Alcoholic Muscle Disease
Epidural Abscess Myasthenia Gravis Subudral Empyema Muscular Dystrophies
Brain Abscess Familial Periodic Paralysis . .
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MENINGITIS

What is Encephalitis and Meningitis?

Encephalitis is an inflammation of the brain. There are many types of encephalitis, most of which are caused by viral infection. Symptoms include sudden fever, headache, vomiting, photophobia (abnormal visual sensitivity to light), stiff neck and back, confusion, drowsiness, clumsiness, unsteady gait, and irritability. Symptoms that require emergency treatment include loss of consciousness, poor responsiveness, seizures, muscle weakness, sudden severe dementia, memory loss, withdrawal from social interaction, and impaired judgement. Meningitis is an infection of the membranes (called meninges) that surround the brain and spinal cord. Symptoms, which may appear suddenly, often include high fever, severe and persistent headache, stiff neck, nausea, and vomiting. Changes in behavior such as confusion, sleepiness, and difficulty waking up are extremely important symptoms and may require emergency treatment. In infants symptoms of meningitis may include irritability or tiredness, poor feeding and fever. Meningitis may be caused by many different viruses and bacteria. Viral meningitis cases are usually self-limited to 10 days or less. Some types of meningitis can be deadly if not treated promptly. Anyone experiencing symptoms of meningitis or encephalitis should see a doctor immediately.

Is there any treatment?
Antiviral medications may be prescribed for herpes encephalitis or other severe viral infections. Antibiotics may be prescribed for bacterial infections. Anticonvulsants are used to prevent or treat seizures. Corticosteroids are used to reduce brain swelling and inflammation. Sedatives may be needed for irritability or restlessness. Over-the-counter medications may be used for fever and headache. Individuals with bacterial meningitis are usually hospitalized and treated with antibiotics. Antiviral drugs may also be prescribed.

What is the prognosis?
The prognosis for encephalitis varies. Some cases are mild, short and relatively benign and patients have full recovery. Other cases are severe, and permanent impairment or death is possible. The acute phase of encephalitis may last for 1 to 2 weeks, with gradual or sudden resolution of fever and neurological symptoms. Neurological symptoms may require many months before full recovery. With early diagnosis and prompt treatment, most patients recover from meningitis. However, in some cases, the disease progresses so rapidly that death occurs during the first 48 hours, despite early treatment.

What research is being done?
The NINDS supports and conducts research on infections and diseases of the brain and nervous system including encephalitis and meningitis. Much of this research is aimed at learning more about the cause(s), prevention, and treatment of these disorders.

Selected references

Pruitt, AA.
Infections of the Nervous System Neurology Clinics 16(2); 419-447 (1998).

Townsend, GC, and Scheld, WM.
Infections of the Central Nervous System Advances in Internal Medicine 43; 403-447 (1998).

Durand, M, et al.
Acute Bacterial Meningitis in Adults. The New England Journal of Medicine, 328:1; 21-28 (January 7, 1993).

Quagliarello, V, and Scheld, W.
Bacterial Meningitis: Pathogenesis, Pathophysiology, and Progress. The New England Journal of Medicine, 327:12; 864-872 (September 17, 1992).

Whitley, R.
Viral Encephalitis The New England Journal of Medicine, 323:4; 241-250 (July 26, 1990)

 Organizations

Meningitis Foundation of America, Inc.
7155 Shadeland Station
Suite 190
Indianapolis, IN 46256-3922
support@musa.org
http://www.musa.org
Tel: 800-668-1129 317-595-6383
Fax: 317-595-6370

National Institute of Allergy and Infectious Diseases (NIAID)
National Institutes of Health
31 Center Drive, Rm. 7A50 MSC 2520
Bethesda, MD 20892-2520
(see website)
http://www.niaid.nih.gov
Tel: 301-496-5717

This fact sheet is in the public domain. You may copy it.

Provided by:
The National Institute of Neurological Disorders and Stroke
National Institutes of Health
Bethesda, MD 20892

LABORATORY FINDINGS

The diagnosis of CNS infection is made primarily by documentation of changes within the CSF obtained by lumbar puncture.  A deep yellow colour of spinal fluid is derived primarily from bilirubin pigment.  In the absence of haemorrhage, this is most frequently associated with elevated protein concentration and may be seen when the CSF circulation has been impaired.  Increased CSF protein generally accompanies an increase in white blood cells (WBC) and is the result of injury to the meninges by an inflammatory process and subsequent passive diffusion of albumin into the CSF from serum.  As few as 200 WBC/ul to 300 WBC/ul impart haziness to CSF; 500 WBC/ul give the CSF an opalescent appearance;  and 700 WBC/ul  to 800 WBC/ul cause a turbid appearance.   Fluid containing thousands of cells will look like pus.
Polymorphonuclear leukocytes predominate in bacterial infections, whereas lymphocytes predominate in tuberculous and nonbacterial infections.  A lack of cells does not invariably exclude the possibility of bacterial meningitis but this certainly is a rare occurrence.  Various stains (Gram's immunofluorescent,  acid-fast, auramine-rhodamine, india ink) and cultures on several media should be done on CSF to identify the pathogenic organism.  There is a decrease in CSF glucose in bacterial, tuberculous, mycotic, and carcinomatous meningitis.
Decreased CSF glucose is the result of increased glucose utilisation by rapidly growing microorganisms, phagocytosis of bacteria by WBC, and impaired glucose transport into the CSF from the bloodstream across the inflammatory exudate.

Acute Bacterial Meningitis

Other Laboratory Findings Tuberculous Meningitis Cryptococcal Meningitis

click on the image to view original.
This is one of a series of Great images to be found on the linked page!
Fig. 2 Pyogenic Meningitis: This photomicrograph of subarachnoid space, in hematoxylin/eosin stain, shows the two components of an acute bacterial meningitis: polymorphonuclear leukocytes and fibrin, the latter arranged in meshes and strands (bottom of picture). The subarachnoid space is compromised, but not completely occluded.

For Original Image from the Virtual Hospital site click this link.
This section was stained with GMS, a silver stain which intensely stains the thick, gelatinous capsule of the cryptococcus. The other finding to note on this slide, which is also typical of fungal infections in the CNS, is the minimal inflammatory response relative to the number of organisms.

VIRAL INFECTIONS

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LABORATORY FINDINGS

CSF

Blood
ACUTE ENCEPHALITIS

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Arboviruses

LABORATORY FINDINGS

CSF

Protein and glucose normal

Skin Biopsy

Protein up to 100 mg/dl
Glucose normal
Bacterial culture negative

Blood

Viral serologic tests show fourfold increase in titre from acute to convalescent sera.
Haemagglutination inhibition and neutralisation antibodies are detected within 1 week after onset of symptoms and persist for at l east 8 years.
Complement-fixation antibodies first appear 2 to 3 weeks after onset and persist for 1 to 3 years.
Isolation of virus from blood and CSF of patients during the acute disease is unusual.

Herpes Simplex Virus

Link to this image no longer works (ref:www.healthcentral.com/ mhc/fullsize/2886.jpg)
Pathogenesis:
Primary infection occurs through a break in the mucus membranes of the mouth or throat, via the eye or genitals or directly via minor abrasions in the skin. because of the universal distribution of the virus, most individuals are infected by 1-2 years of age; initial infection is usually asymptomatic, although there may be minor local vesicular lesions. Local multiplication ensues, followed by viraemia and systemic infection. There then follows life-long latent infection with periodic reactivation. During primary infection, the virus enters peripheral sensory nerves and migrates along axons to sensory nerve ganglia in the CNS - allows virus to escape immune response! During latent infection of nerve cells, viral DNA is maintained as an episome (not integrated) with limited expression of specific virus genes required for the maintenance of latency - true latency.
The delicate balance of latency may be upset by various disturbances, physical (injury, U.V, hormones, etc) or psychological (stress, emotional upset - perhaps affecting immune system/hormonal balance).
Reactivation of latent virus leads to recurrent disease - virus travels back down sensory nerves to surface of body and replicates, causing tissue damage:

LABORATORY FINDINGS

CSF

Brain Biopsy

Click on image for link to original image and an excellent teaching page.
Chronic Inflammation, Viral Encephalitis: Note the brain post capillary venule cuffed by lymphocytes. This is an example of inflammation that arises with an initial lymphocytic response. It is acute in a temporal sense but the infiltrate contains few or no neutrophils. It is sometimes called chronic inflammation simply because of the lymphocytic infiltrate. Certain virus and bacteria preferentially elicit this type of initial response - probably because there are no chemotactic factors for neutrophils present.

Herpes Zoster

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Click here or on image for link to original article
Herpes zoster results from reactivation of the varicella-zoster virus. Unlike varicella (chickenpox), herpes zoster is a sporadic disease with an estimated lifetime incidence of 10 to 20 percent. The incidence of herpes zoster increases sharply with advancing age, roughly doubling in each decade past the age of 50 years. Herpes zoster is uncommon in persons less than 15 years old. In a recent study,1 patients more than 55 years of age accounted for more than 30 percent of herpes zoster cases despite representing only 8 percent of the study population. In this same study, children less than 14 years old represented only 5 percent of herpes zoster cases.

The normal age-related decrease in cell-mediated immunity is thought to account for the increased incidence of varicella-zoster virus reactivation. Patients with disease states that affect cell-mediated immunity, such as human immunodeficiency virus (HIV) infection and certain malignancies, are also at increased risk. Chronic corticosteroid use, chemotherapy and radiation therapy may increase the risk of developing herpes zoster.

The incidence of herpes zoster is up to 15 times higher in HIV-infected patients than in uninfected persons, and as many as 25 percent of patients with Hodgkin's lymphoma develop herpes zoster. The occurrence of herpes zoster in HIV-infected patients does not appear to increase the risk of acquired immunodeficiency syndrome (AIDS) and is less dependent on the CD4 count than AIDS-related opportunistic infections. There is no evidence that herpes zoster heralds the onset of an underlying malignancy.

Race may influence susceptibility to herpes zoster. Blacks are one fourth as likely as whites to develop this condition. Although herpes zoster is not as contagious as the primary varicella infection, persons with reactivated infection can transmit varicella-zoster virus to nonimmune contacts. Household transmission rates have been noted to be approximately 15 percent.

About 20 percent of patients with herpes zoster develop postherpetic neuralgia. The most established risk factor is age; this complication occurs nearly 15 times more often in patients more than 50 years of age. Other possible risk factors for the development of postherpetic neuralgia are ophthalmic zoster, a history of prodromal pain before the appearance of skin lesions and an immunocompromised state.

Pathophysiology
Varicella-zoster virus is a highly contagious DNA virus. Varicella represents the primary infection in the nonimmune or incompletely immune person. During the primary infection, the virus gains entry into the sensory dorsal root ganglia. How the virus enters the sensory dorsal root ganglia and whether it resides in neurons or supporting cells are not completely understood. The varicella-zoster virus genome has been identified in the trigeminal ganglia of nearly all seropositive patients.

The virus remains latent for decades because of varicella-zoster virus­specific cell-mediated immunity acquired during the primary infection, as well as endogenous and exogenous boosting of the immune system periodically throughout life.8 Reactivation of the virus occurs following a decrease in virus-specific cell-mediated immunity. The reactivated virus travels down the sensory nerve and is the cause for the dermatomal distribution of pain and skin lesions.

The pathophysiology of postherpetic neuralgia remains unclear. However, pathologic studies have demonstrated damage to the sensory nerves, the sensory dorsal root ganglia and the dorsal horns of the spinal cord in patients with this condition.

LABORATORY FINDINGS

CSF

Skin Biopsy
Poliomyelitis

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Poliomyelitis
An acute viral infection with a wide range of manifestations, including nonspecific minor illness, aseptic meningitis (nonparalytic poliomyelitis), and flaccid weakness of various muscle groups (paralytic poliomyelitis).

Etiology and Epidemiology
Poliovirus is an enterovirus. Of the 3 immunologically distinct poliovirus serotypes, type 1 is the most paralytogenic and the most common cause of epidemics.
Man is the only natural host for polioviruses. The infection occurs through direct contact and is highly contagious. Extensive use of vaccines has almost eliminated the disease in developing countries.

Pathology and Pathogenesis
Virus enters the mouth and primary multiplication occurs in lymphoid tissues in the oropharynx and intestinal tract, mainly the ileum. Small amounts of virus reach the blood and are carried to other sites in the reticuloendothelial system, where extensive multiplication occurs. Secondary viremia is followed by invasion of the CNS. Viremia lasts several days but disappears by the time of onset, when antibodies have already developed.
The spinal cord and brain are the only sites of significant virus-induced pathology. Factors predisposing to serious neurologic damage include increasing age, recent tonsillectory, inoculations (most often DTP), pregnancy and physical exertion concurrent with onset of the CNS phase.

LABORATORY FINDINGS

CSF

Blood
Slow Virus Infections

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SLOW VIRUS INFECTIONS - Extract from the Merck Manual

Viral infections characterized by long incubations or a prolonged disease course.

Slow or chronic viral infections that result in chronic neurologic disease are caused by conventional viruses (retroviruses, papovaviruses) and prions (unconventional transmissible spongiform encephalopathy agents). In these slowly developing, progressive diseases, clinical manifestations begin months to years after the initial exposure.

Progressive Multifocal Leukoencephalopathy

A subacute progressive, demyelinating CNS disorder that usually occurs as an opportunistic infection in patients with underlying depression of cell-mediated immunity.

Etiology

Progressive multifocal leukoencephalopathy (PML) is thought to be caused by reactivation of the JC virus, a human papovavirus. It is associated with disorders of the reticuloendothelial system, such as leukemia and lymphoma, but may occur in any condition with concomitant depression of cell-mediated immunity (eg, AIDS, Wiskott-Aldrich syndrome, organ transplantation). Today, PML is seen most often as a complication of AIDS. (Currently, 4% of AIDS patients have the condition.) A few cases have occurred in patients without a detectable immune disorder.

Symptoms, Signs, and Diagnosis

Onset may be subacute or gradual, but the course is relentlessly progressive. The duration from onset of symptoms to death is usually 1 to 9 mo. The neurologic findings reflect both focal and diffuse involvement of the cerebral hemispheres. Pyramidal tract involvement manifested by hemiparesis is the most common finding. Aphasia, dysarthria, and hemianopsia are also frequent. Sensory changes and cerebellar and brain stem signs may be present. As focal involvement becomes multifocal, the disease may appear to be diffuse, with progressive intellectual impairment of varying severity in 2/3 of patients. Occasionally, an incomplete or complete transverse myelitis appears. Headaches and convulsive seizures are rare; however, these symptoms have been reported more frequently in patients with AIDS.

MRI and CT scans demonstrate uni- or bilateral, single or multiple lesions in the white matter. On CT, they are nonenhancing low-density lesions. MRI reveals increased signal intensity of T-2 weighted images and T-1 enhanced images in 10 to 15% of cases. CSF studies are usually normal. The EEG commonly shows diffuse and focal abnormalities corresponding to the underlying asymmetric pathology, but these findings are not pathognomonic. Serologic studies do not confirm the diagnosis because 2/3 of the normal population already have antibodies to JC virus, and underlying immunologic abnormalities in most patients with PML make serologic tests unreliable. Newer polymerase chain reaction techniques allow for the detection of a single copy of JC viral DNA in 50 µL of CSF. If necessary, a definitive diagnosis can be made by stereotaxic biopsy. However, this is not recommended except in cases in which the MRI or CT scan indicates an unusual lesion pattern. Diagnosis is confirmed by identifying the JC virus in brain tissue using immunofluorescent antibody staining or electron microscopic agglutination.

Treatment

Anecdotal reports have shown favorable therapeutic responses to cytosine or adenine arabinoside, but a controlled trial in AIDS patients has indicated no benefit. Recently, there have been at least two cases reported in AIDS patients with a favorable outcome after high doses of zidovudine. In these cases, life expectancy was increased > 2 yr.

LABORATORY FINDINGS

CSF

Serum Brain Biopsy
NEUROSYPHILIS

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LABORATORY FINDINGS

Serologic Tests for Syphilis

CSF
EPIDURAL ABSCESS

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LABORATORY FINDINGS
 

CSF Laboratory findings of Underlying conditions
SUBDURAL EMPYEMA

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LABORATORY FINDINGS

CSF

Click on image for link to original image and information

B. EPIDURAL AND SUBDURAL ABSCESS OR EMPYEMA

1. Definitions
:

Abscesses are localized collections of pus. Pyogenic organisms are the infectious agent involved with abscess formation. Empyema describes the accumulation of pus within a space or cavity, again, typically secondary to pyogenic organism infection. Epidural and subdural infections can be called either abscess or empyema
2. Pathogenesis of Subdural Abscess/Empyema:

a. Direct inoculation secondary to trauma, usually of organisms resident in the sinuses (often pneumococcus).

b. Secondary to middle ear infections; organisms may erode directly into either space or spread via venous sinuses.
3. Etiologic agents:
Usually bacteria; streptococcus and staphylococcus are the most common.
4. Pathological changes:
Acutely a purulent exudate; organization later; reactive leptomeningitis; cerebral veins in the subdural space may be affected.
5. Spinal fluid changes:
Reactive meningitis occurs; CSF changes include elevation of protein levels, PMN count, and sometimes pressure. No organisms can be cultured, unless the empyema is accompanied by infection of leptomeninges.
6. Complications:
Space-occupying effects plus edema of brain may lead to herniation and midline shift. Infection may spread into leptomeninges and contaminate cerebrospinal fluid in subarachnoid space.

BRAIN ABSCESS

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LABORATORY FINDINGS

CSF (when meninges are not involved) Laboratory Findings of Underlying Diseases

Click on Image for link to original image and article
Brain Abscess: This photomicrograph shows the early capsule formation around an abscess, several weeks after the infection started. The blue aniline stain demonstrates the collagen which is being produced by fibroblasts derived from newly formed blood vessels. The cavity of the abscess is located towards the right upper corner. Some inflammatory debris is still accumulated on the surface. The surrounding brain tissue is edematous.

DURAL SINUS THROMBOPHLEBITIS

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LABORATORY FINDINGS


REYE'S SYNDROME

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LABORATORY FINDINGS


MULTIPLE SCLEROSIS

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NINDS Multiple Sclerosis Information Page
What is Multiple Sclerosis?
Multiple sclerosis (MS) is a life-long chronic disease diagnosed primarily in young adults. During an MS attack, inflammation occurs in areas of the white matter of the central nervous system (nerve fibers that are the site of MS lesions) in random patches called plaques. This process is followed by destruction of myelin, which insulates nerve cell fibers in the brain and spinal cord. Myelin facilitates the smooth, high-speed transmission of electrochemical messages between the brain, the spinal cord, and the rest of the body. Symptoms of MS may be mild or severe and of long duration or short and appear in various combinations. The initial symptom of MS is often blurred or double vision, red-green color distortion, or even blindness in one eye. Most MS patients experience muscle weakness in their extremities and difficulty with coordination and balance. Most people with MS also exhibit paresthesias, transitory abnormal sensory feeling such as numbness or "pins and needles." Some may experience pain or loss of feeling. About half of people with MS experience cognitive impairments such as difficulties with concentration, attention, memory, and judgment. Such impairments are usually mild, rarely disabling, and intellectual and language abilities are generally spared. Heat may cause temporary worsening of many MS symptoms. Physicians use a neurological examination and take a medical history when they suspect MS. Imaging technologies such as MRI, which provides an anatomical picture of lesions, and MRS (magnetic resonance spectroscopy), which yields information about the biochemistry of the brain. Physicians also may study patients' cerebrospinal fluid and an antibody called immunoglobulin G. No single test unequivocally detects MS. A number of other diseases produce symptoms similar to those seen in MS.

Is there any treatment?
There is as yet no cure for MS. Until recently, steroids were the principal medications for MS. While steroids cannot affect the course of MS over time, they can reduce the duration and severity of attacks in some patients. The FDA has recently approved new drugs to treat MS. The goals of therapy are threefold: to improve recovery from attacks, to prevent or lessen the number of relapses, and to halt disease progression.

What is the prognosis?
The cause of MS remains elusive, but most people with MS have a normal life expectancy. The vast majority of MS patients are mildly affected, but in the worst cases, MS can render a person unable to write, speak, or walk.

What research is being done?
Scientists are looking into the body's autoimmune system, infectious agents, and genetics as culprits in MS. Studies into these areas strengthen the theory that MS is the result of a number of factors rather than a single gene or other agent. Studies use a technique called magnetic resonance imaging (MRI) to visualize the evolution of MS lesions in the white matter of the brain. Studies have shown that MS has no adverse effects on the course of pregnancy, labor, or delivery; in fact, the stabilization or remission of symptoms during pregnancy may be attributable to changes in a woman's immune system that allows her to carry a baby.




This fact sheet is in the public domain. You may copy it.

Provided by:
The National Institute of Neurological Disorders and Stroke
National Institutes of Health

Bethesda, MD 20892






LABORATORY FINDINGS

Increased CSF IgG index (>0.65) = CSF IgG/CSF albumin
                                                      Serum IgG/Serum albumin


EPILEPSY

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LABORATORY FINDINGS
 

Conditions that Cause Seizures and have Associated Laboratory Abnormalities

CEREBRAL INFARCTION

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LABORATORY FINDINGS

Cerebral Thrombosis

Cerebral Embolism
CEREBRAL HAEMORRHAGE

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LABORATORY FINDINGS

Epidural and Subdural Haemorrhage

Subarachnoid Haemorrhage Intracerebral Haemorrhage
BRAIN TUMOURS



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See Description in next section

LABORATORY FINDINGS

CSF

Altered Hypothalamic Hormones (see Chap. 6) Laboratory Findings of the Primary Tumour (when the brain tumour is metastatic)
SPINAL-CORD TUMOURS



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What are Brain and Spinal Tumors?
Brain and spinal cord tumors are abnormal growths of tissue found inside the skull or the bony spinal column, which are the primary components of the central nervous system (CNS). Benign tumors are noncancerous, and malignant tumors are cancerous. The CNS is housed within rigid, bony quarters (i.e., the skull and spinal column), so any abnormal growth, whether benign or malignant, can place pressure on sensitive tissues and impair function. Tumors that originate in the brain or spinal cord are called primary tumors. Most primary tumors are caused by out-of-control growth among cells that surround and support neurons. In a small number of individuals, primary tumors may result from specific genetic disease (e.g., neurofibromatosis, tuberous sclerosis) or from exposure to radiation or cancer-causing chemicals. The cause of most primary tumors remains a mystery. They are not contagious and, at this time, not preventable. Symptoms of brain tumors include headaches, seizures, nausea and vomiting, vision or hearing problems, behavioral and cognitive problems, motor problems, and balance problems. Spinal cord tumor symptoms include pain, sensory changes, and motor problems. The first test to diagnose brain and spinal column tumors is a neurological examination. Special imaging techniques (computed tomography, and magnetic resonance imaging, positron emission tomography) are also employed. Laboratory tests include the EEG and the spinal tap. A biopsy, a surgical procedure in which a sample of tissue is taken from a suspected tumor, helps doctors diagnose the type of tumor.

Is there any treatment?
The three most commonly used treatments are surgery, radiation, and chemotherapy. Doctors also may prescribe steroids to reduce the swelling inside the CNS.

What is the prognosis?
Symptoms of brain and spinal cord tumors generally develop slowly and worsen over time unless they are treated. The tumor may be classified as benign or malignant and given a numbered score that reflects how malignant it is. This score can help doctors determine how to treat the tumor and predict the likely outcome, or prognosis, for the patient.

LABORATORY FINDINGS

CSF


Nodular tumor within spinal cord with surrounding cyst

After resection of tumor nodule-Click on images or for link to source document

GUILLAIN-BARRE SYNDROME



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What is Guillain-Barre Syndrome?

Guillain-Barré (ghee-yan bah-ray) syndrome is a disorder in which the body's immune system attacks part of the peripheral nervous system. The first symptoms of this disorder include varying degrees of weakness or tingling sensations in the legs. In many instances, the weakness and abnormal sensations spread to the arms and upper body. These symptoms can increase in intensity until the muscles cannot be used at all and the patient is almost totally paralyzed. In these cases, the disorder is life-threatening and is considered a medical emergency. The patient is often put on a respirator to assist with breathing. Most patients, however, recover from even the most severe cases of Guillain-Barré syndrome, although some continue to have some degree of weakness. Guillain-Barré syndrome is rare. Usually Guillain-Barré occurs a few days or weeks after the patient has had symptoms of a respiratory or gastrointestinal viral infection. Occasionally, surgery or vaccinations will trigger the syndrome. Thedisorder can develop over the course of hours or days, or it may take up to 3 to 4 weeks. No one yet knows why Guillain-Barré strikes some people and not others what sets the disease in motion. What scientists do know is that the body's immune system begins to attack the body itself, causing what is known as an autoimmune disease. Guillain-Barré is called a syndrome rather than a disease because it is not clear that a specific disease-causing agent is involved Reflexes such as knee jerks are usuallylost. Because the signals traveling along the nerve are slower, a nerve conduction velocity (NCV) test can give a doctor clues to aid the diagnosis. The cerebrospinal fluid that bathes the spinal cord and brain contains more protein than usual, so a physician may decide to perform a spinal tap.
Is there any treatment?

There is no known cure for Guillain-Barre syndrome, but therapies can lessen the severity of the illness and accelerate the recovery in most patients.

LABORATORY FINDINGS

CSF*
ALCOHOLIC MUSCLE DISEASE

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LABORATORY FINDINGS


MYASTHENIA GRAVIS

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Myasthenia gravis is the most common primary disorder of neuromuscular transmission. The disorder typically strikes between the ages of 20 and 50, with women developing symptoms younger and men developing symptoms later.  Unlike many other neurological disorders, myasthenia gravis does not cause progressive muscle atrophy (wasting away or degeneration).  The disorder can be caused by an acquired immunologic abnormality or by a genetic abnormality.

Symptoms

Initially, people with myasthenia gravis may complain about specific muscle weakness, particularly in the eyes, face and neck.  They may have difficulty swallowing, chewing or speaking, and may have double vision. They also may feel fatigue, especially later in the day. Symptoms can be aggravated by emotional stress, systemic illness such as a viral respiratory infection, menstrual cycle, pregnancy, hypothyroidism or hyperthyroidism, and other factors.

LABORATORY FINDINGS


MUSCULAR DYSTROPHIES

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LABORATORY FINDINGS
 

Early:  Moderate increase in LDH4, marked increase in LDH5
Progressing:  Moderate increases in LDH4 and LDH5
Late:  Moderate increases in LDH3 and LDH4; normal LDH5

Click on Image for link to MD page

Muscular Dystrophies and Myopathies

Myopathies are diseases of the muscles.  They can be caused by an inherited genetic abnormality (as in muscular dystrophy) or an abnormality of the immune system (such as polymyositis).  These disorders can develop at any time from birth through adulthood.  University of Chicago neurologists have expertise in treating many different muscle diseases.

There are many types of muscular dystrophy (MD). These diseases are classified according to the muscle groups involved and the age of onset.  Some of these muscular dystrophies result in premature death; others may allow the person to live for decades with varying degrees of disability.

Symptoms 

Muscular dystrophy is characterized by muscle weakness in various parts of the body, depending on the type of MD or myopathy.  Muscle weakness progresses (worsens) over time.  Initial symptoms usually develop gradually.


FAMILIAL PERIODIC PARALYSIS


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Familial periodic paralysis

Alternative names:

hypokalemic periodic paralysis; periodic paralysis - familial; periodic paralysis - hypokalemic

Definition:

A disorder that occurs within certain families and causes intermittent episodes of >muscle weakness

Causes, incidence, and risk factors:

Familial periodic paralysis is a condition of intermittent episodes ofparalysis or muscle weakness that occurs in multiple members of a family group. Many (but not all) cases of familial periodic paralysis are termed "hypokalemic" periodic paralysis.

Hypokalemic periodic paralysis occurs as an inherited condition. In most cases, it is inherited as an autosomal dominant disorder (only one parent must transmit the gene). In other cases, the disorder appears sporadically in a family group.

The disorder involves attacks of muscle weakness or paralysis alternating with periods of normal muscle function. Attacks usually begin in adolescence but can occur before age 10. Attacks of intermittent weakness that do not begin until adulthood are rare and usually caused by other disorders. The frequency of attacks varies from daily to yearly. Episodes of muscle weakness may last for a few hours or persist for several days.

During an attack of muscle weakness, there is a low level of potassium in the bloodstream (serum). Serum potassium levels are normal between attacks. There is no decrease in total body potassium, however. Potassium flows from the bloodstream into muscle cells. Insulin levels may affect the disorder in some people because insulin increases the flow of potassium into cells.

Weakness most commonly affects the muscles of the arms and legs but may occasionally affect the eye muscles or the muscles involved in breathing and swallowing (which can be fatal). Although muscle strength is initially normal between attacks, repeated attacks may eventually cause progressive and persistent muscle weakness between attacks.

Risks include a family history of periodic paralysis. Attacks may be triggered by ingestion of high carbohydrate meals. Attacks most commonly occur after sleep or rest and are rare during exercise, but rest after an exercise period may trigger an attack. The risk is slightly higher in Asian men who also have thyroid disorders thyrotoxic periodic paralysis.

Disorders that cause intermittent episodes of paralysis as their primary effect are uncommon. Familial periodic paralysis occurs in approximately 1 out of 100,000 people. Men are affected more often than women and usually have more severe symptoms.

LABORATORY FINDINGS
 

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