VIEWS: 51 PAGES: 4 POSTED ON: 7/4/2009
1. Summarize all the neurological findings and make a clinicoanatomic correlation (Neurological Localization) The following are the neurologic signs and symptoms manifested by the patient: Hemiplegia (paralysis) on the right arm, leg, and central face Hypotonia on the right extremities, as manifested by 0/5 MRC muscle strength grade Hypoflexia on the right extremities Dorsiflexion plantar response (Babinski’s sign) on the right foot Tongue deviated to the right on protrusion Preferential gaze to the left Dysarthia (difficulty talking) Hemiplegia or paralysis of the right arm and leg was the first neurologic symptom experienced by the patient. This was then followed by hemiplegia or paralysis on the right central face. This manifestation could have resulted from a lesion in the posterior limb of the internal capsule. A lesion in the posterior limb of the internal capsule disrupts the influence of the cerebral cortex on the lower motorneurons on the contralateral side of the body. The corticospinal and corticobulbar tracts are affected, and so with the rubrospinal and reticulospinal pathways. Immediately following such a lesion, the patient develops paralysis of the face, arm, and leg (hemiplegia) of the opposite side of the body, with hypotonia and depression of the muscle stretch reflexes (hypoflexia), which were also manifested by the patient. Therefore, since the hemiplegia, hypotonia, and hypoflexia were manifested on the right side of the patient, then the lesion could be on the left posterior limb of the internal capsule. The corticospinal (pyramidal) tract consists of upper motorneurons in the cerebral cortex with axons coursing through the pyramidal tract in the medulla and terminating on anterior horn cells or interneurons in the spinal cord. An important neurologic sign that clearly can be attributed selectively to lesions to the corticospinal tract is Babinski’s sign, which was also seen in the patient. A corticospinal tract lesion rostral to the level of the pyramidal decussation gives rise to contralateral spasticity, muscle weakness, and Babinski’s sign. A lesion of this tract caudal to the level of the pyramidal decussation (i.e., in the spinal cord) causes these signs on the ipsilateral side of the body. With regards to the patient, the corticospinal tract lesion is rostral to the level of the pyramidal decussation. Several of the individual cranial nerves pass close to the pyramidal tract before they emerge from the brain stem. A single lesion that includes the nerve and the tract at this point produces loss of function of the cranial nerve on the side of the lesion and a contralateral hemiplegia. As in the case of the patient, a lesion on the left hypoglossal nerve and the left pyramid results in paralysis of the muscles of the left half of the tongue, which explains the deviation of the tongue to the right on protrusion, and right hemiplegia; resulting in the disturbance in the execution of speech (dysarthia) in the patient. The lesions in the posterior limb of the internal capsule and the corticospinal tract result from the blockage of the middle cerebral artery (MCA). The middle cerebral artery is a terminal branch of the internal carotid. It enters the depth of the lateral fissure and divides into cortical branches that spread in a radiating fashion to supply the insula and the lateral surface of the frontal, parietal, occipital, and temporal lobes. The lateral and medial striate arteries, sometimes termed lenticulostriate arteries, are small branches that come from the basal part of the middle cerebral artery and the anterior cerebral artery to supply the internal capsule and portions of the basal ganglia. Blockage of the lateral striate arteries by atherosclerosis causes infarction of the internal capsule that manifests as stroke. If the entire MCA is occluded at its origin (blocking both its penetrating and cortical branches) and the distal collaterals are limited, the clinical findings are contralateral hemiplegia, hemianesthesia, homonymous hemianopia, and a gaze preference to the ipsilateral side, as manifested by the patient. 2. Based on the temporal profile, make an initial impression. Cite and justify at least 3 differential diagnoses. Judging from the previously stated neurological localization, my initial impression is Ischemic Stroke secondary to occlusion of the Left Middle Cerebral Artery. Ischemic strokes are caused by thrombosis or embolism and accounts for approximately 85% of all strokes. Ischemic strokes most often are caused by extracranial embolism, intracranial thrombosis, and by the reduction in the cerebral blood flow. Neurologic symptoms are manifest within 10 seconds because Acute ischemic stroke refers to strokes caused by thrombosis or embolism and accounts for 85% of all strokes. On the macroscopic level, ischemic strokes most often are caused by extracranial embolism or intracranial thrombosis, but they may also be caused by decreases in cerebral blood flow. On the cellular level, any process that disrupts blood flow to a portion of the brain unleashes an ischemic cascade, leading to the death of neurons and cerebral infarction. Within seconds to minutes of the loss of perfusion to a portion of the brain, an ischemic cascade is unleashed that, if left unchecked, causes a central area of irreversible infarction surrounded by an area of potentially reversible ischemic penumbra. On the cellular level, the ischemic neuron becomes depolarized as ATP is depleted and membrane ion-transport systems fail. The resulting influx of calcium leads to the release of a number of neurotransmitters, including large quantities of glutamate, which, in turn, activates N-methyl-D-aspartate (NMDA) and other excitatory receptors on other neurons. These neurons then become depolarized, causing further calcium influx, further glutamate release, and local amplification of the initial ischemic insult. This massive calcium influx also activates various degradative enzymes, leading to the destruction of the cell membrane and other essential neuronal structures. Free radicals, arachidonic acid, and nitric oxide are generated by this process, which leads to further neuronal damage. Within hours to days after a stroke, specific genes are activated, leading to the formation of cytokines and other factors that in turn cause further inflammation and microcirculatory compromise. Ultimately, the ischemic penumbra is consumed by these progressive insults, coalescing with the infracted core, often within hours of the onset of the stroke. Differential Diagnoses: Transient Ischemic Attack (TIA) A transient ischemic attack (TIA) is an acute episode of temporary and focal loss of cerebral function of vascular (occlusive) origin. TIAs are rapid in onset; symptoms reach their maximal manifestation in fewer than 5 minutes (usually <1 min). Manifestations are of variable duration and typically last 2-15 minutes (rarely as long as 24 h). Most TIA durations are less than 1 hour; median duration is 14 minutes in the carotid distribution and 8 minutes in vertebrobasilar ischemia. Temporary reduction or cessation of cerebral blood flow adversely affects neuronal function in cortical, subcortical, and nuclear regions of the CNS. Polyneuropathy (Diabetic Polyneuropathy) Polyneuropathy is a term used to describe the clinical syndrome resulting from diffuse lesions of peripheral nerves. Muscular weakness and atrophy accompanied by sensory loss in the extremities are characteristic of this disorder. These symptoms were manifested by the patient, hence, this differential is considered. Furthermore, the muscle stretch reflexes usually are diminished or absent in the affected portions of the limbs. And lastly, one of the frequent causes of polyneuropathy includes diabetes mellitus, and the patient is a diagnosed diabetic. However, this differential is made less likely by the fact that in polyneuropathy, the lesions often are manifested bilaterally, and this was not the case of the patient. The patient manifested weakness, paralysis, and hypoflexia only on the right side of the body. Moreover, in this disorder, the distribution of the symptoms occur in a so-called “glove-and-stocking” fashion, which means that distal parts of the extremities are affected more than the proximal parts. In the case of the patient, weakness and paralysis occur all throughout the extremities. Diabetic peripheral neuropathy is the presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after exclusion of other causes. Peripheral neuropathies have been described in patients with primary (types 1 and 2) and secondary diabetes of diverse causes, suggesting a common etiologic mechanism based on chronic hyperglycemia. The contribution of hyperglycemia has received strong support from the Diabetes Control and Complications Trial (DCCT). The dose dependent effect of hyperglycemia on nerves has been supported further in recent years by increasing recognition of an association between impaired glucose tolerance (prediabetes) and peripheral neuropathy. Pathologically, numerous changes have been demonstrated in both myelinated and unmyelinated fibers. The factors leading to the development of peripheral neuropathy in diabetes are not understood completely, and multiple hypotheses have been advanced. It is generally accepted to be a multifactorial process. The best-supported mechanisms include the following: The Metabolic Theory proposes that hyperglycemia causes increased levels of intracellular glucose in nerves, leading to saturation of the normal glycolytic pathway. Extra glucose is shunted into the polyol pathway and converted to sorbitol and fructose by the enzymes aldose reductase and sorbitol dehydrogenase. Accumulation of sorbitol and fructose lead to reduced nerve myoinositol, decreased + + membrane Na /K -ATPase activity, impaired axonal transport, and structural breakdown of nerves, causing abnormal action potential propagation. This is the rationale for the use of aldose reductase inhibitors to improve nerve conduction. According to the Vascular (ischemic-hypoxic) theory, endoneurial ischemia develops because of increased endoneurial vascular resistance to hyperglycemic blood. Various metabolic factors, including formation of advanced glycosylation end products, also have been implicated. The end results are + + capillary damage, inhibition of axonal transport, reduced Na /K -ATPase activity, and finally axonal degeneration. According to the altered neurotrophic support theory, neurotrophic factors are important in the maintenance, development, and regeneration of responsive elements of the nervous systems. Nerve growth factor (NGF) is the best studied. This protein promotes survival of sympathetic and small-fiber neural crest–derived elements in the peripheral nervous system. In animals with diabetes, both production and transport of NGF are impaired. Antioxidants have been used to enhance the effects of NGF. According to the Laminin theory, laminin is a large, heteromeric, curariform glycoprotein composed of a large alpha chain and two smaller beta chains, beta 1 and beta 2. In cultured neurons, laminin promotes neurite extension. Lack of normal expression of the laminin beta 2 gene may contribute to the pathogenesis of diabetic neuropathy. Autoimmune diabetic neuropathy is postulated to result from immunogenic alteration of endothelial capillary cells. This is the basis for the use of intravenous immunoglobulin (IVIg) to treat some variants of diabetic neuropathy. Diabetic polyneuropathy often develops as generalized asymptomatic dysfunction of peripheral nerve fibers. The first clinical sign that usually develops in tandem with abnormal nerve conductions is decrease or loss of ankle jerks, or decrease or loss of vibratory sensation over the great toes. With more severe involvement, the patient may lose deep tendon reflexes and develop weakness of small foot muscles. More focal findings may be seen with injury to specific nerves as described above. There are five criteria which are needed to establish the diagnosis of diabetic polyneuropathy. The patient has diabetes mellitus by National Diabetes Data Group criteria. Diabetes mellitus has caused prolonged chronic hyperglycemia. The patient has predominantly distal sensorimotor polyneuropathy in the lower extremities. Diabetic retinopathy or nephropathy is approximately similar in severity to polyneuropathy. Other causes of sensorimotor polyneuropathy have been excluded. Guillain-Barre Syndrome GBS is a heterogeneous grouping of immune-mediated processes generally characterized by motor, sensory, and autonomic dysfunction. In its classic form, GBS is an acute inflammatory demyelinating polyneuropathy characterized by progressive symmetric ascending muscle weakness, paralysis, and hyporeflexia with or without sensory or autonomic symptoms; however, variants involving the cranial nerves or pure motor involvement are not uncommon. In severe cases, muscle weakness may lead to respiratory failure, and labile autonomic dysfunction may complicate the use of vasoactive and sedative drugs. Although the clinical syndrome classically presents as a rapidly progressive acute polyneuropathy, several pathologic and etiologically subtypes exist. Most patients with GBS exhibit absent or profoundly delayed conduction in action nerve fibers. This aberrant conduction results from demyelination of nerve cell axons. Peripheral nerves and spinal roots are the major sites of demyelination, but cranial nerves also may be involved. GBS is believed to result from an autoimmune response, both humoral and cell mediated, to a recent infection or any of a long list of medical problems. Its relation to antecedent infections and the identification of various antiganglioside antibodies suggest that molecular mimicry may serve as a possible mechanism for the disease. The antibodies formed against gangliosidelike epitopes in the lipopolysaccharide layer of some infectious agents have been shown in both necropsy and animal models to cross-react with the ganglioside surface molecules of peripheral nerves. Symptoms generally coincide pathologically with various patterns of lymphocytic infiltration and macrophage-mediated demyelination, depending on the subtype in question. Recovery is typically associated with remyelination. In a subset of patients, GBS is associated primarily with myelin-sparing axonal damage resulting from a direct cellular immune attack on the axon itself.
Pages to are hidden for
"Stroke case2"Please download to view full document