Neurology is a branch of medicine dealing with disorders of the nervous system. Physicians specializing in the field of neurology are called neurologists and are trained to diagnose, treat, and manage patients with neurological disorders. Most neurologists are trained to treat and diagnose adults. Pediatric neurologists, nearly always a subspecialty of pediatrics, treat neurological disease in children.

Field of work

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Neurological disorders are disorders that affect the central nervous system (brain, brainstem and cerebellum), the peripheral nervous system (peripheral nerves - cranial nerves included), or the autonomic nervous system (parts of which are located in both central and peripheral nervous system). Neurologists also diagnose and treat some conditions in the musculoskeletal system.

Major conditions include:

• headache disorders such as migraine, cluster headache and tension headache
• epilepsy and seizure disorders
• neurodegenerative disorders, the most common class being dementias, including Alzheimer's disease
• cerebrovascular disease, such as transient ischemic attacks, and strokes (ischemic or hemorrhagic)
• sleep disorders
• cerebral palsy
• infections of the central nervous system (encephalitis), brain envelopes (meningitis) and peripheral nerves (neuritis), such as brain abscess, herpetic meningoencephalitis, aspergilloma, cerebral hydatic cyst
• some infections of the peripheral nervous system, such as tetanus and botulism
• neoplasms - tumors of the brain and its envelopes (brain tumors), spinal cord tumors, tumors of the peripheral nerves (neuroma)
• movement disorders such as Parkinson's disease, chorea, hemiballismus, tic disorder, and Gilles de la Tourette syndrome
• demyelinating diseases of the central nervous system, such as multiple sclerosis, and of the peripheral nervous system, such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP)
• spinal cord disorders - tumors, infections, trauma, malformations (e.g., myelocele, meningomyelocele, tethered cord)
• disorders of peripheral nerves, muscle (myopathy) and neuromuscular junctions
• traumatic injuries to the brain, spinal cord and peripheral nerves
• altered mental status, encephalopathy, stupor and coma

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Archives of Neurology recent issues

Urate as a Predictor of the Rate of Clinical Decline in Parkinson Disease [Original Contribution]
Ascherio, A., LeWitt, P. A., Xu, K., Eberly, S., Watts, A., Matson, W. R., Marras, C., Kieburtz, K., Rudolph, A., Bogdanov, M. B., Schwid, S. R., Tennis, M., Tanner, C. M., Beal, M. F., Lang, A. E., Oakes, D., Fahn, S., Shoulson, I., Schwarzschild, M. A., for the Parkinson Study Group DATATOP InvestigatorsBackground  The risk of Parkinson disease (PD) and its rate of progression may decline with increasing concentration of blood urate, a major antioxidant.Objective  To determine whether serum and cerebrospinal fluid concentrations of urate predict clinical progression in patients with PD.Design, Setting, and Participants  Eight hundred subjects with early PD enrolled in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism (DATATOP) trial. The pretreatment urate concentration was measured in serum for 774 subjects and in cerebrospinal fluid for 713 subjects.Main Outcome Measures  Treatment-, age-, and sex-adjusted hazard ratios (HRs) for clinical disability requiring levodopa therapy, the prespecified primary end point of the original DATATOP trial.Results  The HR of progressing to the primary end point decreased with increasing serum urate concentrations (HR for highest vs lowest quintile = 0.64; 95% confidence interval [CI], 0.44-0.94; HR for a 1-SD increase = 0.82; 95% CI, 0.73-0.93). In analyses stratified by -tocopherol treatment (2000 IU/d), a decrease in the HR for the primary end point was seen only among subjects not treated with -tocopherol (HR for a 1-SD increase = 0.75; 95% CI, 0.62-0.89; vs HR for those treated = 0.90; 95% CI, 0.75-1.08). Results were similar for the rate of change in the Unified Parkinson's Disease Rating Scale score. Cerebrospinal fluid urate concentration was also inversely related to both the primary end point (HR for highest vs lowest quintile = 0.65; 95% CI, 0.44-0.96; HR for a 1-SD increase = 0.89; 95% CI, 0.79-1.02) and the rate of change in the Unified Parkinson's Disease Rating Scale score. As with serum urate concentration, these associations were present only among subjects not treated with -tocopherol.Conclusions  Higher serum and cerebrospinal fluid urate concentrations at baseline were associated with slower rates of clinical decline. The findings strengthen the link between urate concentration and PD and the rationale for considering central nervous system urate concentration elevation as a potential strategy to slow PD progression.Published online October 12, 2009 (doi:10.1001/archneurol.2009.247).
Autoimmune Targets of Heart and Skeletal Muscles in Myasthenia Gravis [Original Contribution]
Suzuki, S., Utsugisawa, K., Yoshikawa, H., Motomura, M., Matsubara, S., Yokoyama, K., Nagane, Y., Maruta, T., Satoh, T., Sato, H., Kuwana, M., Suzuki, N.Objective  To investigate the clinical, histological, and immunological features of patients with myasthenia gravis (MG) who also developed myocarditis and/or myositis.Design  Observational and retrospective case series.Setting  Keio University, Hanamaki General Hospital, Kanazawa University, Nagasaki University, and Juntendo University.Patients  A cohort of 8 patients with MG with clinically defined inflammatory myopathies.Interventions  Clinical and histological features were described. Serological analyses included MG-related antistriational autoantibodies (those to titin, ryanodine receptor, muscular voltage-gated potassium channel Kv1.4) and myositis-specific autoantibodies.Results  Of 924 patients with MG, 8 (0.9%) had inflammatory myopathies. The mean (SD) onset age of MG was 55.3 (10.3) years. All patients showed severe symptoms with bulbar involvement; 5 patients had myasthenic crisis and 4 had invasive thymoma. Myocarditis was found in 3 patients and myositis in 6. Myocarditis, developing 13 to 211 months after the MG onset, was characterized by heart failure and arrhythmias. Myositis, developing before or at the same time as MG, affected limb and paraspinal muscles. Histological findings of skeletal muscles showed CD8+ lymphocyte infiltration. Seven patients had 1 of these antistriational autoantibodies but not myositis-specific autoantibodies. Immunomodulatory therapy was required for all patients and was effective for both MG and inflammatory myopathies, although 1 patient died.Conclusions  Heart and skeletal muscles are autoimmune targets in some patients with MG. This autoimmunity has a broad clinical spectrum with antistriational autoantibodies.Published online September 14, 2009 (doi:10.1001/archneurol.2009.229).
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