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Neurological Disorders - Disease Topic Overview

Neurology is the branch of medicine dealing with all diseases of the nervous system, including those of the brain, spinal cord and nerves.¹

The nervous system is a highly specialised and complex structure.² It is an information-processing system that regulates all physiological functions of the body.² When a disease affects this system, it can result in difficulty moving, speaking, breathing or problems with memory or behaviour.²

There are more than 600 neurological disorders; the most common are Alzheimer's disease (dementia), Parkinson's disease, migraine and epilepsy.³

Alzheimer's disease is a neurodegenerative disease that causes progressive and irreversible loss of mental functions, such as memory, language, orientation and judgment.³ Usually diagnosed from the age of 65, it is the leading cause of dementia and dependency in elderly, and affected about 24 million people worldwide in 2005 according to the World Health Organisation.³

Parkinson's disease is a neurodegenerative disease characterised by tremors when muscles are at rest, slowness of voluntary movements and increased muscle tone (rigidity).⁴ It is often diagnosed after 65 and affects 1% of people of this age bracket.⁴

Migraine is one of the most prevalent neurological disorders, affecting up to 18% of the population.5 Migraine is characterised by attacks of severe unilateral head pain, associated with nausea, vomiting, phonophobia, and photophobia.5

Epilepsy is a chronic neurological disorder affecting both sexes, regardless of age or country of origin.³ Epilepsy consists a set of neurological conditions characterised by the occurrence of at least one epileptic seizure.⁶ Epileptic seizure is a sudden symptom, characterized by abnormal brain hyperactivity. It may manifest as seizures or unconsciousness, or even visual or auditory hallucinations.⁶

Neurological diseases, especially neurodegenerative diseases like Alzheimer's or Parkinson's disease, remain incurable with a poorly understood etiology. With the population aging, neurological diseases are a major health problem, particularly for developing countries where life expectancy increases dramatically.³ Studies are ongoing to identify risk factors that would allow better prevention of neurological diseases, pending the development of effective treatments.³

1. Reinhard Rohkamm R. Color atlas of neurology. Thieme editionedition. 2004 : 440 pages.
2. Michael-Titus A. et al. The nervous system. Elsevier Editionedition. 2007 : 371 pages.
3. World Health Organization. Neurological disorders: Ppublic health challenges. WHO editionedition. 2006 : 218 pages. Available online.
4. Beers M.H. et al. The Merck manual of medical information. Merck research laboratories. Second home edition. 2003, : 431-96.
5. Zaza Katsarava Z. The many facets of migraine. The Lancet Neurology. July 2011 ; 10 (7) : 607.
6. Fisher R.S. et al. Eepileptic seizures and epilepsy: Ddefinitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia. 2005 ; 46 (4) : 470–472.

Alzheimer's Disease
Alzheimer's disease(AD) is a progressive, neurodegenerative disease which will affect most of us at one point in time, and it’s prevalence increases with age.

In the early stages in particular, dementia is often difficult to diagnose, since many symptoms are not recognized as such or are trivialized by the patient. 20% of actual dementia cases are reported to be incorrectly diagnosed as a different disease.

In early dementia the symptoms of Alzheimer’s disease include memory loss, disorientation and confusion. These symptoms are caused by the loss of neurons and worsen with continuous neurodegeneration. The pathology of dementia is not solely the result of a cholinergic deficit. It is known that, chronically and pathologically elevated glutamate concentrations play an important role.

In general two main groups of dementia can be distinguished, requiring different types of treatment:
- Cerebro-organic (primary) forms of dementia
- Non-cerebro-organic (secondary) forms of dementia
Depending on the stage of the disease, clinical symptoms of varying intensity dominate. With the progression of AD, treatment is aimed particularly at improving and stabilizing personal everyday functions, so as to keep patients independent for as long as possible.

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Alzheimer's disease (AD) is a progressive, neurodegenerative disease which will affect most of us at one point in time - either directly (as the prevalence is expected to quadruple over the next 50 years) or indirectly through the suffering of a loved one.

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ADHD

Attention-deficit hyperactivity disorder (ADHD) is a heterogeneous neurobehavioural disorder characterised by inattention, hyperactivity and impulsivity.¹ ADHD is one of the most common neurobehavioural disorders of childhood,^1,2 but can continue to cause impairment throughout adolescence and into adulthood.³

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Attention-deficit hyperactivity disorder (ADHD) is a heterogeneous neurobehavioural disorder characterised by inattention, hyperactivity and impulsivity.¹ ADHD is one of the most common neurobehavioural disorders of childhood,^1,2 but can continue to cause impairment throughout adolescence and into adulthood.³

Learn more about ADHD… by visiting the ADHD Institute

Diagnosis of ADHD often occurs based on the history of ADHD symptoms, which usually develop before the age of 7 years⁴ and are often first noticed in the school setting. This is because the characteristic symptoms of inattention, impulsivity and hyperactivity are problematic in social and school environments.⁵ Teachers in particular may be very well placed to identify ADHD symptoms when children start school.⁶ Symptoms can persist through adolescence and into adulthood.⁷

Learn more about the diagnosis of ADHD…

The aim of treatment is to manage the symptoms of ADHD and improve psychological, social, educational and occupational functioning.⁸ In this respect, treatment should encompass pharmacological and behavioural approaches. Due to the chronic nature of ADHD, a management programme should be put in place that takes into account the need for treatment and monitoring over time.⁹ A guide to managing ADHD may involve setting out desired improvements following discussions with the patient, the treating clinician and, if appropriate, parents, carers and school teachers. It may also be appropriate to set goals for treatment.⁹

Learn more about the treatment options for patients with ADHD…

A range of additional resources are also available. These include; a discussion forum , ADHD Institute meetings, congress reports, a congress calendar and useful links.

References:
1. Remschmidt H. Global consensus on ADHD/HKD. Eur Child Adolesc Psychiatry 2005; 14: 127-137.
2. Brown RT, Freeman WS, Perrin JM, et al. Prevalence and assessment of attention-deficit/hyperactivity disorder in primary care settings. Pediatrics 2001; 107: e43.
3. Pliszka S, AACAP Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry 2007; 46: 894-921.
4. American Psychiatric Association (APA). Diagnostic and Statistical Manual of Mental Disorders Fourth Edition (Text Revision): DMS-IV-TR.
5. Faraone SV, Doyle AE. The nature and heritability of attention-deficit/hyperactivity disorder. Child Adolesc Psychiatr Clin N Am 2001; 10: 299-316, viii-ix.
6. National Institute for Health and Clinical Excellence (NICE). Attention deficit hyperactivity disorder: diagnosis and management of ADHD in children, young people and adults, 2008. Available from http://www.nice.org.uk/nicemedia/pdf/CG072NiceGuidelinev4.pdf. Accessed 1 October 2010.
7. Faraone SV, Biederman J, Mick E. The age-dependent decline of attention deficit hyperactivity disorder: a meta-analysis of follow-up studies. Psychol Med 2006; 36: 159-165.
8. American Academy of Pediatrics. Subcommittee on Attention-Deficit/Hyperactivity Disorder and Committee on Quality Improvement. Clinical practice guideline: treatment of the school-aged child with attention-deficit/hyperactivity disorder. Pediatrics 2001; 108: 1033-1044.
9. Quinlan DM. Assessment of attention deficit/hyperactivity disorder and comorbidities. In: Brown TE (Ed). Attention-deficit Disorders and Comorbidities in Children, Adolescents, and Adults (1st ed). Washington, DC: American Psychiatric Press Inc, 2000.

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Migraine
Migraine is a common neurological disorder characterised by recurrent episodes of headache pain with associated symptoms including nausea, vomiting, sensitivity to light and sound, and, in a minority of patients, transient neurological symptoms, with visual disturbances being the most common.

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Migraine is a severe, episodic disorder with freedom from symptoms between attacks. Attacks are characterised by transient focal neurological symptoms, headache, or both.

Correctly diagnosing a migraine headache enables prompt and appropriate therapeutic intervention, reducing the distress and pain experienced by patients. An incorrect diagnosis of migraine can have a significant effect on both migraineurs and their families.

Several sets of guidelines have been developed to assist in the diagnosis of migraine.

Among migraineurs, understanding and assessing the severity and disability of a patient’s illness is an important step in ascertaining their treatment needs.

The Migraine Disability Assessment (MIDAS) questionnaire is a self-administered form that assesses the impact that migraine has on a patient’s work and social life. It can be used prior to and at the time of an initial consultation and throughout treatment to monitor the patient’s progress.

The use of a headache diary, which allows patients to record events that play a role in their headaches, is also a useful tool that may aid the physician in the diagnosis of migraine.

Despite the availability of migraine-specific medications such as the triptans, which are effective and well tolerated for the acute treatment of migraine, many migraineurs lapse from physician care before being prescribed an effective treatment.

It is advised that users of this resource consult their local treatment guidelines before initiating any treatment programme for a patient with migraine. Once migraine is diagnosed, patients and physicians should decide together how best to treat acute attacks and whether to use preventive medications.

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Multiple Sclerosis
The hallmark of multiple sclerosis (MS) as revealed by magnetic resonance imaging (MRI) is the white matter plaque, which represents an area of demyelination and axonal loss. MS can produce lesions throughout the central nervous system (CNS).

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The hallmark of multiple sclerosis (MS) as revealed by magnetic resonance imaging (MRI) is the white matter plaque, which represents an area of demyelination and axonal loss.

MS can produce lesions throughout the central nervous system (CNS), but certain sites appear to be especially vulnerable, such as the optic nerve, brain stem, spinal cord and periventricular regions. Involvement is often bilateral and symmetrical. Lesions are broadly divided into two types: acute and chronic.

Acute lesions are inflammatory in nature and exhibit infiltration by T-lymphocytes, B-lymphocytes and macrophages, which may be filled with myelin debris from the breakdown of myelin sheaths. Proliferation of astrocytes is also usually evident, accompanied by oligodendrocyte loss.

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Niemann-Pick type C
Niemann-Pick type C disease is a rare genetic lysosomal storage disorder that causes severe, progressive neurological symptoms. It is a very serious, life-threatening condition that can affect infants, children and adults. NP-C is characterized by cellular accumulation of lipids, in particular unesterified cholesterol and glycosphingolipids, in many parts of the body including brain, liver and spleen.

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Niemann-Pick type C disease is a rare genetic lysosomal storage disorder that causes severe, progressive neurological symptoms. It is a very serious, life-threatening condition that can affect infants, children and adults. NP-C is characterized by cellular accumulation of lipids, in particular unesterified cholesterol and glycosphingolipids, in many parts of the body including brain, liver and spleen.

The variability of NPC presentations provides a wide range of life expectancy. In general, early-onset patients tend to die during childhood or early adolescence, while patients with later-onset disease who appear to be less drastically affected can live into late adulthood.

Accurate diagnosis of NPC requires awareness of many clinical phenotypes, narrowing of differential diagnosis by ancillary testing and final confirmation by biochemical testing – the current mainstay of primary diagnosis in NPC.

The prevalence of NPC has undoubtedly been underestimated in the past due to a mixture of factors including confusing terminology, prior lack of specific biochemical or genetic tests, varied pathology, and the many variant clinical manifestations of the disease.

Current, non-specific treatments for NPC focus mainly on supportive care, aimed toward managing the symptoms of the disease. As such, these treatments have no effect on disease progression or long-term outcomes.

Specific therapies for the intended treatment of NPC are based on targeting known pathophysiological and/or biochemical defects involved in the pathogenesis of the disease. While earlier attempts proved largely ineffective, more recent efforts indicate possible hope for the future.

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Parkinson's Disease
Parkinson's disease (PD) is a progressive, degenerative disorder of the central nervous system, which causes increasing disability over time. PD predominantly occurs in people over the age of 50 and is the commonest neurodegenerative disorder after Alzheimer's disease that a physician will encounter.

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Parkinson's disease (PD) is a degenerative disorder of the central nervous system characterized by the clinically asymmetric onset of resting tremor, bradykinesia, rigidity and postural instability.^1-3

Parkinson's disease (PD) is the second most common neurodegenerative disorder, after Alzheimer's disease.^{1, 2}

The most recent and comprehensive clinical guidelines for the diagnosis and management of Parkinson's disease (PD) in primary and secondary care have been compiled by the UK National Institute for Health and Clinical Excellence (NICE).⁴

A diagnosis of Parkinson's disease (PD) can be difficult as, in common with other central nervous system degenerative disorders, PD begins insidiously.

The severity of Parkinson's disease (PD) can be assessed using a number of rating scales, assessing patients' motor function, activities of daily living (ADL), mental status, dependency and complications of therapy.

It is important that patients with Parkinson's disease (PD) are treated as soon as a full diagnosis has been made; several studies have shown that patients who receive effective symptomatic treatment earlier in the course of their disease fare significantly better clinically than patients who delay their treatment.^5-7

It is not possible to identify a universal first-choice drug therapy for patients with early PD.⁸ In Established/advanced Parkinson's disease⁹ therapy choices need to be re-evaluated.

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References

1. de Lau, L.M. and M.M. Breteler, Epidemiology of Parkinson's disease. Lancet Neurol, 2006. 5(6): p. 525-35.
2. Schapira, A.H., Science, medicine, and the future: Parkinson's disease. BMJ, 1999. 318(7179): p. 311-4.
3. Guttman, M., S.J. Kish, and Y. Furukawa, Current concepts in the diagnosis and management of Parkinson's disease. CMAJ, 2003. 168(3): p. 293-301.
4. NICE, N.I.f.H.a.C.E., NICE clinical guideline: Parkinson's disease: diagnosis and management in primary and secondary care. 2006.
5. Schapira, A.H. and J. Obeso, Timing of treatment initiation in Parkinson's disease: a need for reappraisal? Ann Neurol, 2006. 59(3): p. 559-62.
6. Poewe, W.H. and G.K. Wenning, The natural history of Parkinson's disease. Neurology, 1996. 47(6 Suppl 3): p. S146-52.
7. Rajput, A.H., Levodopa prolongs life expectancy and is non-toxic to substantia nigra. Parkinsonism Relat Disord, 2001. 8(2): p. 95-100.
8. Horstink, M., et al., Review of the therapeutic management of Parkinson's disease. Report of a joint task force of the European Federation of Neurological Societies and the Movement Disorder Society-European Section. Part I: early (uncomplicated) Parkinson's disease. Eur J Neurol, 2006a. 13(11): p. 1170-85.
9. Horstink, M., et al., Review of the therapeutic management of Parkinson's disease. Report of a joint task force of the European Federation of Neurological Societies (EFNS) and the Movement Disorder Society-European Section (MDS-ES). Part II: late (complicated) Parkinson's disease. Eur J Neurol, 2006b. 13(11): p. 1186-202.

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Soft Tissue Sarcoma
Soft Tissue Sarcomas (STS) are malignant (cancerous) tumors that develop in tissues which connect, support, or surround other structures and organs of the body. Muscles, tendons (bands of fiber that connect muscles to bones), fibrous tissues, fat, blood vessels, nerves, and synovial tissues are types of soft tissue.

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Soft Tissue Sarcomas (STS) are malignant (cancerous) tumors that develop in tissues which connect, support, or surround other structures and organs of the body. Muscles, tendons (bands of fiber that connect muscles to bones), fibrous tissues, fat, blood vessels, nerves, and synovial tissues are types of soft tissue.

Soft tissue sarcomas are grouped together because they share certain microscopic characteristics, have similar symptoms, and are generally treated in similar ways¹. They are usually named for the type of tissue in which they begin.

Every year approximately 13,000 new cases of soft tissue sarcomas are diagnosed in adults and children in Europe. The 5-year survival rate for patients with soft tissue sarcoma is around 90% if the cancer is detected in early phases and before it has spread. However, the 5-year survival rate is 10% to 15% for sarcomas with metastasis.

Management of STS depends on the stage of disease and histological subtype². Surgery is the mainstay of treatment for patients with localised disease and is often curative. However, as recurrence is likely to occur when tumour cells remain after surgery, adjuvant radiotherapy is often also considered, especially for patients with intermediate or high-grade tumours. Radiotherapy is also often administered for patients in whom surgery is inappropriate or who decline surgery.²

There are a number of Associations and Organisations across Europe who strive to inform others of this disease as well as offer help and support to those affected or to those who know and want to help those suffering.

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References

1. Cormier JN, Pollock RE. Soft tissue sarcomas. CA: A Cancer Journal for Clinicians 2004; 54(2):94–109.
2. Clark MA, Fisher C et al. (2005) “Soft-tissue sarcomas in adults.” N Engl JMed 353(7): 701–11.

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Latest Journal Publications

Journal of the neurological sciences

A 73-year-old man had episodic encephalopathy, ataxia and neuropathy. Symptoms largely resolved but adenopathy later lead to the diagnosis of a low-grade follicular lymphoma. The neurological symptoms soon recurred with new pontine calcifications identified by computed tomography. Brain biopsy revealed microvascular endothelial cell nuclear changes. Electron microscopy identified small polymorphic bacteria without a cell wall and with terminal and attachment organelles within endothelial cells and clustered in some microvascular lumina. Immunostaining was positive for Mycoplasma pneumoniae and convalescent serum enzyme immunoassay was positive for M. pneumoniae IgG. The patient again recovered and he was neurologically stable 33months after the initial episode. The ultrastructural findings of the bacterial cells are distinctive of some mycoplasmal species when compared to other small bacteria. Mycoplasma-like organisms are reported in four autopsied patients who had chronic encephalopathy, movement disorders, and some of the same light- and electron-microscopic findings in the brain as our patient. Direct neuroinvasion by Mycoplasma species has been suggested, while anatomic observations in our patient and in the four autopsy cases show microvascular invasion but not parenchymal invasion. Most mycoplasmal encephalitis may be immune-mediated. The frequency of neurovascular invasion is not known. It may be rare and it may persist.

Journal of Experimental Child Psychology

Speech perception of four phonetic categories (voicing, place, manner, and nasality) was investigated in children with specific language impairment (SLI) (n = 20) and age-matched controls (n = 19) in quiet and various noise conditions using an AXB two-alternative forced-choice paradigm. Children with SLI exhibited robust speech perception deficits in silence, stationary noise, and amplitude-modulated noise. Comparable deficits were obtained for fast, intermediate, and slow modulation rates, and this speaks against the various temporal processing accounts of SLI. Children with SLI exhibited normal “masking release” effects (i.e., better performance in fluctuating noise than in stationary noise), again suggesting relatively spared spectral and temporal auditory resolution. In terms of phonetic categories, voicing was more affected than place, manner, or nasality. The specific nature of this voicing deficit is hard to explain with general processing impairments in attention or memory. Finally, speech perception in noise correlated with an oral language component but not with either a memory or IQ component, and it accounted for unique variance beyond IQ and low-level auditory perception. In sum, poor speech perception seems to be one of the primary deficits in children with SLI that might explain poor phonological development, impaired word production, and poor word comprehension.

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