Hemiplegia - Study Guide

Summary: Hemiplegia for Medical Students

Here is a summary of the information about hemiplegia based on the provided sources, organized into 'Must Memorize' and 'Important Concepts to Understand' sections for a medical student.

The sources discuss hemiplegia primarily in the context of Cerebrovascular Disease (Stroke). While a precise definition of hemiplegia isn't explicitly provided, it is described as a type of paralysis resulting from lesions affecting the nervous system. It is a significant consequence of stroke, which is noted as the leading cause of severe neurologic disability in adults.

Must Memorize:

• Hemiplegia is a type of paralysis.
• It results from lesions affecting the pyramidal tract along its course.
• Stroke is the most common cause. Strokes can be ischemic (∼ 85%) or hemodilated (∼ 15%). Stroke is the leading cause of severe neurologic disability in adults.
• Common sites of lesions causing hemiplegia include the Cerebral cortex, Sub cortical regions, Capsule, Brain stem (mid brain, pons, medulla), and Spinal cord up to segment 5.
• Signs of Upper Motor Neuron (UMN) type paralysis, characteristic of hemiplegia above the spinal cord level, include:
  • Increased muscle tone (spasticity).
  • Exaggerated deep reflexes.
  • Positive Babinski sign.
  • Lost abdominal and cremasteric reflexes on the affected side.
• Capsular lesions are the commonest cause of hemiplegia at this specific location. They typically result in complete hemiplegia. Associated signs often include hemi hypesthesia on the paralyzed side and UMN facial and hypoglossal palsy on the same side of paralysis. Crucially, capsular lesions typically do not cause convulsions, aphasia, or coma.
• Brain stem lesions cause crossed hemiplegia. This is characterized by hemiplegia on the opposite side of the lesion and Lower Motor Neuron (LMN) cranial nerves affection on the same side of the lesion (opposite to the hemiplegia).
• Spinal cord lesions (specifically affecting the pyramidal tract up to segment 5) cause ipsilateral hemiplegia below the level of the lesion. At the level of the lesion, there may be ipsilateral LMN weakness, loss of reflexes mediated by interrupted segments, and radicular loss of sensation. Below the level, there is ipsilateral deep sensory loss and contralateral superficial sensory loss.
• The onset of hemiplegia can vary based on etiology: usually acute in hemorrhage, may be subacute in thrombosis, sudden in embolic, gradual in neoplasm, and intermittent in D.S. (Multiple Sclerosis).
• Differential diagnoses for stroke (a common cause of acute focal neurological deficits like hemiplegia) include Brain tumors, Chronic subdural hematoma, Encephalitis, and Brain abscess.
• The initial and most used investigation for acute focal neurological deficits suggestive of stroke is Non contrast CT Brain to immediately exclude mimics like intracranial hemorrhage or masses.
• For acute ischemic stroke, Thrombolysis with recombinant tissue plasminogen activator (rt-PA) is a key treatment, with a critical golden time window of 3-4.5 hours from symptom onset.
• Treatment for acute hemorrhagic stroke includes managing blood pressure, treating raised intracranial pressure, and potentially surgical intervention for large or symptomatic hematomas.

Important Concepts to Understand:

• The clinical presentation of hemiplegia varies significantly depending on the site of the lesion in the nervous system and its etiology. Understanding the anatomy of the pyramidal tract and surrounding structures at different levels is crucial for localization.
• Lesions in the Cerebral cortex may result in incomplete hemiplegia or monoplegia due to the wide origin of the pyramidal tract. They can also be associated with cloudiness of consciousness, sensory loss (if parietal lobe is involved), convulsions, and higher mental function disorders depending on the specific area affected.
• Subcortical lesions produce similar symptoms to cortical lesions but with potentially more extensive weakness.
• Hemiplegia is usually of the UMN type below the level of the lesion, resulting in characteristic signs like spasticity and hyperreflexia. However, spinal cord lesions at the level of the lesion can cause LMN signs, and brainstem lesions involve cranial nerves which are LMNs.
• Investigations are typically directed at identifying the underlying cause, such as imaging studies (CT, MRI, angiography) for stroke or tumors and potentially laboratory tests or lumbar puncture depending on the suspected etiology (e.g., infection, metabolic causes, inflammatory conditions).
• Treatment focuses on addressing the underlying cause (e.g., reperfusion therapy for ischemic stroke, surgical intervention for tumors or certain hematomas, antibiotics for infections). Supportive care and managing complications are also essential.
• Rehabilitation measures should be initiated early, particularly after stroke, to help patients recover function.
• Conditions like congenital cerebral palsy or hysterical paralysis can also present with paralysis. Hysterical paralysis is noted as having no organic pyramidal tract lesion.