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Transcranial B-mode sonography (TCS) is a widely available, non-invasive and cost-effective diagnostic instrument. By convention and due to the resolution of the ultrasound waves in proximity of the probe, structures that are close to the midline are assessed from the ipsilateral side whereas structures that are located distant to the midline are examined from the contralateral side. Most data on TCS in disorders associated with insomnia or parasomnias have been evaluated from the movement disorder perspective and did not address diagnosis or differential diagnosis of sleep disorders directly. Some interesting findings indicate that TCS is valuable for the evaluation of sleep disorder patients with suspected restless legs syndrome (RLS), depressive disorder, or rapid eye movement (REM) sleep behavior disorder (RBD). In a patient complaining about disturbed sleep a TCS demonstrating substantia nigra (SN) hypoechogenicity, raphe hypoechogenicity, and red nucleus (RN) hyperechogenicity may help to support a suspected diagnosis of RLS.
Parkinson's and related movement disorders
Daniela Berg, Hertie Institute for Clinical Brain Research, Institute for Medical Genetics, Tübingen, Germany,
Olaf Riess, Institute for Medical Genetics, Tübingen, Germany,
Peter Riederer, Clinic and Policlinic of Psychiatry and Psychotherapy, University of Wurzburg, Germany
Although the primary pathology and key defects of neurotransmission leading to the clinical picture of Parkinson's disease (PD) are known, initiation and nature of the neurodegenerative process are still obscure. However, it is becoming increasingly evident that the underlying pathophysiology is complex and in most cases probably multifactorial, differing among the individuals affected.
Only a very small percentage of Parkinsonian cases are caused by monogenic alterations (see Chapter 40). However, since the first description of a family in which 79 of 194 members suffered from PD (Mjörnes, 1949), it has become evident that the risk of developing the clinical picture of PD is three to four times higher in individuals with relatives with PD compared to those with a negative family history. Functional neuroimaging proved to be especially valuable for the detection of affected siblings: for monozygotic twins a concordance of 75% for PD or at least a subclinical dopaminergic deficit was detected by PET-studies, the rate for dizygotic was 22% (Piccini et al., 1999). These and other findings provide strong evidence of a genetic contribution to idiopathic PD (Gasser et al., 1998, 2001). However, only about 25% of PD patients report a relative affected by the same disease. Therefore, other factors are necessary to explain the selectivity and susceptibility of the disease on the basis of a genetic predisposition. Biochemical and histological investigations of the past decades have illuminated some of these factors.
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