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Ataxia is the most important sign of cerebellar disease, but there are other potential causes of ataxia. Postural and limb tremor are additional signs of cerebellar disease. Patients with cerebellar disorders may walk with a wide-based, staggering gait, making it seem as if they were intoxicated by alcohol. Frontal lobe disorders might cause cerebellar-like symptoms with walking difficulties and clumsiness. Frontal lobe lesions are commonly associated with impairment of cognitive function and changes in personality, and often cause urinary incontinence. Lesions of the cerebellar hemisphere are followed by ipsilateral limb ataxia including hypotonia in acute lesions, and if the dentate nucleus is involved, kinetic tremor. Vascular lesions of the cerebellum itself and of the corticopontocerebellar and dentatothalamic pathways might result in ataxia. Limb ataxia and ataxia of gait are common in superior cerebellar artery (SCA), the posterior inferior cerebellar artery (PICA), and the anterior inferior cerebellar artery (AICA) territory infarctions.
According to the criteria of the International Headache Society (IHS), a migraine is defined as a disease with periodic occurring headache episodes, typically associated with autonomic symptoms. The release of neuropeptides explains the actual origin of pain but not how and why the attack begins so abruptly in humans. Triptans improves the typical additional symptoms like nausea or vomiting, photo- and photophobia, and improves the ability to return to work. During a migraine attack, most patients suffer from gastrointestinal symptoms. The aim of migraine prophylaxis is a reduction of frequency, severity and duration of migraine attacks and the prevention of medication overuse headache. Effective for preventive migraine therapy are the non-selective beta-blocker propranolol and the beta-1-selective beta-blocker metoprolol. Most psychological treatments used in migraine therapy are behavior therapies. Paroxysmal pain of short duration located in a region of one of the trigeminus nerves is very characteristic for the trigeminal neuralgia.
Secondary prevention aims at preventing a stroke after a transient ischemic attack (TIA) or a recurrent stroke after a first stroke. About 80–85% of patients survive a first ischemic stroke [1, 2]. Of those between 8% and 15% suffer a recurrent stroke in the first year. Risk of stroke recurrence is highest in the first few weeks and declines over time [3–5]. The risk of recurrence depends on concomitant vascular diseases (CHD, PAD) and vascular risk factors and can be estimated by risk models [6, 7]. Stroke risk after a TIA is highest in the first 3 days . Therefore immediate evaluation of patients with stroke or TIA, identification of the pathophysiology and initiation of pathophysiology based treatment is of major importance . In the following sections, we will deal with the treatment of risk factors, antithrombotic therapy and surgery or stenting of significant stenosis of extra- or intracranial arteries. Each paragraph will be introduced by recommendations, followed by the scientific justification.
Treatment of risk factors
Antihypertensive therapy reduces the risk of stroke. The combination of an ACE inhibitor (perindopril) with a diuretic (indapamide) was significantly more effective than placebo, and an angiotensin-receptor blocker (ARB, eprosartan) was more effective than a calcium-channel blocker (nitrendipin). Ramipril reduces vascular events in patients with vascular risk factors.
Early initiation of antihypertensive therapy with telmisartan on top of the usual antihypertensive therapy is not more effective than placebo.
Most likely all antihypertensive drugs are effective in secondary stroke prevention. Beta-blockers (atenolol) show the lowest efficacy. More important than the choice of a class of antihypertensives is to achieve the systolic and diastolic blood pressure targets (<140/90 mmHg in non-diabetics and <130/80 in diabetics). In many cases this requires combination therapy. Concomitant diseases (kidney failure, congestive heart failure) have to be considered.
Bürger's disease or thromboangiitis obliterans (TAO) is a nonatherosclerotic segmental inflammatory obliterative vascular disease that affects medium- and small-sized arteries as well as superficial veins. Bürger's disease manifested in the brain has the following morphologic characteristics: arterial occlusions caused by thrombosis in small arteries without arteriosclerosis, and spatial predilection for the cerebral surface in the watershed region between the middle cerebral, anterior, and posterior cerebral arteries. TAO is characterized by claudication or ischemia of both legs and less so of the arms. The disease begins distally and progresses more proximally. The diagnosis of TAO requires the exclusion of an embolic source, autoimmune disease, diabetes, and hyperlipidemia. Arteriography should show the distal involvement with normal arterial lumen proximal to the popliteal or distal brachial level and the absence of atheromatous changes in the large vessels. Abstinence from tobacco will likely halt disease progression and sometimes result in regression of vascular changes.
The term ‘ataxia’ (Greek, a- (= negative article) + taxi (= order), (‘lack of order’) is commonly used synonymously with incoordination (Dow & Moruzzi, 1958; Gilman et al., 1981; Timmann & Diener, 1998). Ataxia is the most important sign of cerebellar disease. Cerebellar ataxia is defined as lack of accuracy or coordination of movement which is not due to paresis, alteration in tone, loss of postural sense or the presence of involuntary movements (DeJong, 1979). Cerebellar ataxia relates to motor dysfunctions of the limbs, trunk, eyes, and bulbar musculature. Ataxia of gait refers to incoordination of walking, which might be so severe that the patient cannot walk (abasia). Postural ataxia refers to ataxia of stance and sitting and includes truncal ataxia.The patient may be unable to sit or stand without support (astasia). Limb ataxia refers to incoordination of limb movements and ataxia of speech to cerebellar dysarthia.
Cerebellar disease results in postural and limb tremor. There may be a rhythmic tremor of the body that can evolve into a severe titubation. Limb tremor occurs as a kinetic and to a lesser extent static tremor. Kinetic tremor occurs as an oscillatory movement when the subject initiates a movement of the limb or during the course of moving the limb. The tremor becomes more prominent as the moving limb approaches a target (intention tremor). Powerful, but brief involuntary movements at the beginning of the movement are due to intention myoclonus, not tremor, and occur in diseases involving the dentate nucleus or the superior cerebellar peduncle.
Neurological findings in cerebellar disease
Patients with cerebellar disorders walk with a wide-based, staggering gait, making it seem as if they were intoxicated by alcohol.
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