Diagnostic Tests for MELAS
MELAS Tests: Book Excerpts
Home Diagnostic Testing
These home medical tests may be relevant to MELAS:
- Brain & Neurological Disorders: Related Home Testing:
MELAS Diagnosis: Book Excerpts
Diagnostic Tests for MELAS: Online Medical Books
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ACIDOSIS (DECREASED PH):
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
This should include a CBC, chemistry panel, electrolytes, arterial blood gas analysis, serum and urine ketones, lactic acid, pulmonary function tests, EKG, and consultation with a pulmonologist or nephrologist.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
LACTIC DEHYDROGENASE ELEVATION:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The diagnostic workup should include a CBC, urinalysis, chemistry panel, sedimentation rate, ANA, urine and serum creatine, urine myoglobin, serial EKGs, blood gas analysis, LDH isoenzymes, chest x-ray, lung scan, EMG, and cardiology and neurology consults. A liver scan, CT scan of the abdomen and liver, and muscle biopsy may be necessary.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Stroke:
Physical examination (PE)
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. General examination. This should include vital signs (notably blood pressure), Mini-Mental Status Examination, and an examination of the eyes, including funduscopic. A screening neurologic examination of cranial nerves, coordination, muscle strength, sensation, deep tendon, reflexes, and gait is recommended.
B. Additional PE. Evaluate the heart (arrhythmia, mitral stenosis) and vascular system (carotid bruits), and palpate the scalp and neck (trauma and migraine) and superficial temporal arteries (arteritis).
Testing
A. Clinical laboratory tests. In most instances, laboratory tests are not helpful in the acute assessment. Laboratory tests that may be suggested by the clinical history and PE include blood sugar, coagulation studies (prothrombin, partial thromboplastin times), platelet count, antiphospholipid antibodies, protein S, protein C, antithrombin III, and toxicology screens (cocaine, amphetamines). C-Reactive protein can be of prognostic significance (4). Additional tests may be relevant, depending on the history and PE, including electrocardiogram, cardiac monitoring, electroencephalogram, and spinal tap.
B. Diagnostic imaging. In most instances, diagnostic imaging should include an emergent cerebral CT scan of the brain to rule out abscess, tumor, or hemorrhage. A magnetic resonance imaging scan is a better test for aneurysm, arteriovascular malformation, or tumors. Other tests can include transthoracic or esophageal echocardiogram, duplex carotid ultrasonography, cerebral angiography, and magnetic resonance angiography.
Diagnostic assessment.
The key to the diagnosis of stroke is the duration of neurologic event coupled with the signs and symptoms. The CT scan rules out other serious pathology that can mimic stroke. Specifically, laboratory tests can aid in the workup and are directed by the history and physical examination.
References
1. Schneck MJ. Acute stroke: an aggressive approach to intervention and prevention. Hosp Med 1998;34(1):11–28.
2. Graffagnino C, Itaachinski V. Stroke (brain attack). In: Dambro MR, ed. Griffith’s 5-minute clinical consult, 2nd ed. Philadelphia: Lippincott, Williams & Wilkins, 1999:1014–1015.
3. Nendaz MR, Sarasin FP, Junod AF. Preventing stroke recurrence in patients with patent foramen ovale: antithrombotic therapy, foramen closure, or therapeutic abstention? A decision analytic perspective. Am Heart J 1998;135(3):532–541.
4. Muir KW, Weir CJ, Alwan W. C-Reactive protein and outcome after ischemic stroke. Stroke 1999;30:981–985.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Stroke Syndromes:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
Brain ischemia leading to stroke may be due to embolism from carotid or cardiac sources, systemic hypoperfusion, or in situ thrombosis. Embolic strokes occur suddenly with maximal focal deficits at the onset. Rapid improvement favors an embolic TIA. Thrombosis symptoms fluctuate in a stepwise pattern. Intracerebral hemorrhage progresses gradually over minutes to hours. Aneurysmal subarachnoid hemorrhage occurs in an instant, and focal brain dysfunction is usually absent. Strokelike symptoms due to migraine are recognized by a headache, epiphenomena such as anorexia/nausea and photophobia, and occurrence in younger patients.
A TIA proceeds to stroke in 10% to 40%. Risk is especially high in “crescendo TIA,” which is usually caused by an ulcerated carotid plaque. Amaurosis fugax (“a shade coming down” or transient monocular loss of vision) is a classic presentation. Amaurosis fugax, an anterior circulation event, should be distinguished from transient hemianopsia, a posterior circulation event. An asymptomatic carotid bruit is an imperfect indicator of carotid stenosis and subsequent stroke risk, with an annual risk of an ipsilateral stroke not preceded by a TIA of 1% to 3% per year.
Examination of the optic fundus may reveal a cholesterol crystal, white platelet-fibrin or red clot emboli. Subhyaloid hemorrhage often accompanies a subarachnoid or intracerebral hemorrhage. A red patch with a white center (Roth spot) may be seen in bacterial endocarditis. With occlusion of the carotid artery, the iris may appear speckled and the ipsilateral pupil dilated and poorly-reactive.
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Source: Field Guide to Bedside Diagnosis, 2007

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