Stroke, cause syndromes

Suggested Alternatives for Differential Diagnosis Bartonellosis, brucellosis, other causes of encephalitis, coxsackieviruses, cryptococcosis, cysticercosis, cytomegalovirus, histoplasmosis, legionellosis, leptospirosis, listeria, lyme disease, malaria, rabies, tuberculosis, mumps, stroke, metabolic encephalopathy, Reye syndrome, Bartonella infection, Naegleria infection, Ebstein-Barr virus, prion disease, toxic ingestions, and AIDS. 

The cause of Alzheimer s disease is unknown, but genetic factors clearly play a role. One clue supporting this view is provided by the observation that individuals with Down syndrome, a common cause of mental retardation, frequently develop a dementia similar to Alzheimer s disease during early adulthood. Vascular dementia, which is also called multi-infarct dementia, results from the accumulation of tiny strokes. Individually, these strokes or infarcts are too small to cause any noticeable problem, but as they accumulate, they produce deficits similar to Alzheimer s disease. Other neurological diseases such as Parkinson s disease, Pick s disease, and Huntington s disease cause slow deterioration of the brain that ultimately leads to a degenerative dementia. 

Brain lesions that produce depression can be divided into structural and biochemical types. Any disease that produces a mass lesion or deficit in the frontal lobes can cause a depressive syndrome. Typically, occurrence and severity are correlated with proximity to the tip of the frontal lobe rather than to the extent of motor function loss. The most extensively studied lesions are strokes, but tumors and plaques related to multiple sclerosis can both produce similar results. 

Diabetes mellitus is a heterogeneous group of syndromes characterized by an elevation of fasting blood glucose that is caused by a relative or absolute deficiency in insulin. Diabetes is the leading cause of adult blindness and amputation and a major cause of renal failure, heart attack, and stroke. The disease can be classified into two groups, type 1 and type 2. 

The anti-phospholipid syndrome refers to a range of autoimmune conditions which are characterised by venous or arterial thrombosis, recurrent strokes, pulmonary embolism, recurrent pregnancy loss or obstetric complications and the presence of circulating antibodies with specificity to a range of phospholipids including phosphatidylserine and cardiolipin. The syndrome is the leading cause of vascular thrombosis in children. It sometimes accompanies other autoimmune conditions such as systemic lupus erythematosus (SLE). 

Chronic diseases caused by physical inactivity and inappropriate diet consumption are epidemic in modem Western society. Chronic diseases develop over a lifetime, with clinical sequelae occurring many years after the underlying pathogenesis of the disease has occurred. As we move ahead in the 21st century, cardiovascular diseases (i.e., coronary artery disease, hypertension, stroke, and heart failure), type 2 diabetes, metabolic syndrome, and cancer are the leading killers in Western society and are increasing dramatically in developing nations. 

Cll. Chomyn, A., Enriquez, J. A., Micol, V., Fernandez-Silva, P., and Attardi, G., The Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episode syndrome-associated human mitochondrial 1 k A1 11 k i mutation causes aminoacylation deficiency and concomitant reduced association of mRNA with ribosomes. J. Biol. Chem. 275, 19198—19209 (2000). 

In the CURE study, 12,562 patients with acute coronary syndromes without ST-segment elevation have received ASA and clopidogrel 300 mg bolus, followed by 75 mg daily, versus ASA and placebo (50). The clopidogrel group had early reduction [within 24 hours of treatment—9.3% vs. I 1.4%, RR reduction 20% (p < 0.001) in the primary endpoint death from cardiovascular cause, nonfatal Ml, or stroke], which was sustained at one year, and was observed in all patients with acute coronary syndromes regardless of their level of risk. CURE patients who underwent PCI and were randomized to clopidogrel had a 31% RR reduction in death and Ml compared with placebo-treated PCI patients (51). 

Transient ischemic attack (TIA) is a clinical syndrome characterized by focal neurological symptoms presumed to be of vascular origin that last less than 24 h. Despite the transient nature of symptoms, the cerebrovascular thread is not over yet following a TIA. The mechanism that has given rise to the transient spell may also cause more severe ischemic syndromes if not properly treated. About 10% of patients with TIA suffer from stroke within the ensuing 3 months, 50% of which occur within the first 2 days (Johnston et al. 2003). Accurate and prompt recognition of ischemia as the cause of neurological symptoms is imperative to prevent subsequent strokes. This is, however, a complicated task... 

While physicians may not recognize up to 80% of lacunes (Tuszynski et al. 1989), several clinical syndromes have been correlated with relevant lacunes detected at subsequent autopsy. Five of these are regarded as the classic lacunar syndromes pure motor hemiparesis, sensorimotor stroke, pure sensory hemiparesis, dysarthria clumsy hand syndrome, and ataxic hemiparesis (Donnan et al. 2002 Fisher 1982 Bamford 2001). Pure motor stroke is the commonest lacunar syndrome in clinical practice, while pure sensory stroke is encountered less frequently. The involvement of the face, arm and leg of one side is the characteristic feature of the first three syndromes while reductions of consciousness, cognitive or visual field defects are absent. Even though lacunar infarcts have been linked to lacunar syndromes, the latter are of course not specific for this stroke subtype and mimicked by cortical infarcts, intracerebral hematomas, and non-vascular causes (Bogousslavsky et al. 1988 Bamford 2001). 

This was systematically studied with DWI in 62 consecutive patients who presented with a classic lacunar syndrome (Ay et al. 1999). DWI showed subsidiary acute lesion(s) in addition to the index lacunar lesion in ten patients (16%). The additional lesions were punctuate and lay within the leptomen-ingeal arterial territories in the majority. Patients with subsidiary infarction(s) more frequently harbored an embolic cause of stroke. This finding is critical because underlying embolic cause may give rise to recurrent strokes with more extensive brain injury. Identification of subsidiary infarctions on DWI should have an impact in prompting the physician to introduce the best effective treatment for secondary stroke prevention in a patient with lacunar infarction. 

DWI promises to have tremendous value in accurately localizing the subcortical or brainstem lesion(s). A summary of studies of DWI in patients with lacunar stroke is provided in Table 13.2. It is noteworthy that there is also a group of patients with lacunar infarction who harbor multiple chronic white matter lesions on the conventional MRI and present with non-specific syndromes that could not be attributed to a specific arterial territory. Such symptoms include worsening of a preexisting dysarthria, dysphagia or ataxia, sudden appearance of emotional incontinence or recent onset bowel or bladder problems. Excellent diagnostic performance of DWI in lacunar infarctions may help to prove ischemia as the cause of non-specific neurological symptoms in such patients. 

Subcortical white matter infarcts may mimic a superficial MCA infarct causing a partial anterior circulation syndrome or present as a lacunar syndrome (pure motor, ataxic hemiparesis or sensori motor stroke). Superficial perforating artery infarcts (medullary branches) are often accompanied by cortical spotty lesions. Borderzone and white matter medullary branches infarctions are usually caused by hypoperfusion due lo large vessel occlusion or stenosis (Bogousslavsky 1993 Donnan and Yasaka 1998), but white matter medullary branches infarction can also be caused by cardioembolism (Lee et al. 2003). 

Hypothermia is known to cause cardiac dysfunction, particularly arrhythmias (36,37). Careful temperature control and optimal antiar-rhythmic therapy can minimize this problem. However, to avoid severe circulatory dysfunction, knowledge of arrhythmias is required. Hypothermia may be associated with a suppression of the immunological system, which exposes patients to the danger of severe infections. Schwab et al. reported that 7 of 25 stroke patients undergoing hypoth-ermiatherapy suffered a septic syndrome (17). In our hypothermic study, none of the 13 patients who underwent hypothermia therapy for 3-7 d developed severe infectious diseases. However, the remaining patient, who underwent 10 d of hypothermia because of massive cerebral edema, developed septic shock on the 10th day of hypothermia treatment. The immunosuppressive effect appears to be correlated with the depth and... 

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