Stroke
STROKE (cerebro vascular accident (CVA). Is the sudden loss of neurological function caused by an interruption of the blood flow to the brain.
Ischemic Stroke:
Is the most common type, affecting about 80% of individuals with stroke, and results when a clot blocks or impairs blood flow, depriving the brain of essential oxygen and nutrients.
Hemorrhagic Stroke:
Occurs when blood vessels rupture, causing leakage of blood in or around the brain. Clinically a variety of focal deficits are possible , including changes in the level of consciousness and impairments of sensory, motor, cognitive, perceptual, and languages functions. More deficits are characterized by paralysis( HEMIPLEGIA) or weakness(HEMIPERESIS), typically on the side of the body opposite the side of the lesion. The term Hemingway is often used generally to refer to the wide variety of motor problems that results from stroke.
Anterior Cerebral Artery Syndrome
● Signs and symptoms:
● Contralateral hemiperesis involving mainly the lower extremity ( upper extremity is more spared).
● Contralateral hemisensory loss involving mainly the lower extremity ( upper extremity is more spared).
● Problems with imitation and bimanual tasks, apraxia.
● Contralateral grasp reflex,sucking reflex can be asymptomatic if circle of Willis is competent.
● SIGNS:
● Sudden numbness or weakness in the face, arm, or leg,especially on one side of the body.
● Sudden confusion, trouble speaking or difficulty understanding speech.
● Sudden trouble seeing in one or both eyes .
● Sudden trouble walking dizziness, loss of balance or lack of co_ ordination.
● Sudden severe headche with no known cause.
Middle Cerebral Artery Syndrome
● The middle cerebral artery (MCA) is the second of the two main branches of the internal carotid artery and supplies the entire lateral aspect of the cerebral hemisphere ( frontal,temporal, and parietal lobes) & subcortical structures, including the internal capsule ( posterior portion) , corona radiata, globus pallidus ( Outer part), most of the caudate nucleus , and the Putman.
● Occlusion of the proximal MCA produces extensive neurological damage with significant cerebral edema.
● Increased intracranial pressures typically lead to loss of consciousness, brain herniation ,and possibly death.
● The most common characteristics of MCA syndrome are Contralateral spastic hemiperesis and sensory loss of the face, upper extremity (UE) and lower extremity ( LE), with the face and UE more involved than the LE.
SIGNS AND SYMPTOMS:
● Contralateral hemiparesis involving mainly the UE & face ( LE is more spared)
● Contralateral hemisensory loss involving mainly the UE & face ( LE is more spared)
● Motor speech impairment: broca’s or non_ fluent aphasia with limited vocabulary and slow, hesitant speech.
● Global aphasia : it is caused by damage to the left side of the brain that affects receptive and expressive language skills
● ( needed for both written and oral language)non_ fluent speech with poor comprehension.
● Contralateral homonyms hemianopsia
● Loss of conjugate gaze to the opposite side.
● Ataxia of contralateral limb ( sensory ataxia).
● Pure motor heniplegia( lacuna stroke).
Internal Carotid Artery Syndrome
● Occlusion of the internal carotid artery ( ICA) typically produces massive infarction in the region of the brain supplied by the middle cerebral artery.
● The ICA supplies both the MCA & ACA .
● If collateral circulation to the ACA from the circle of Willis is absent , extensive cerebral infarction in the areas of both the ACA & MCA can occur.
● Significant edema is common with possible uncal herniation, coma and death ( mass effect).
Posterior Cerebral Artery Syndrome
● The two posterior cerebral arteries(PCAs) arise as terminal branches of the basilar artery and each supplies the corresponding occipital lobe and medial and inferior temporal lobe.
● It also supplies the upper brainstem, midbrain, and posterior diencephalon, including most of the thalamus.
● Occlusion proximal to the posterior communicating artery typically results in minimal deficits owing to the collateral blood supply from the posterior communicating artery.
● Occlusion of thalamic branches may produce hemianesthesia ( contralateral sensory loss) or central post stroke ( thalamic ) pain.
SIGNS AND SYMPTOMS:
PERIPHERAL TERRITORY:
● Contralateral homonymous hemianopsia.
● Bilateral homonymous hemianopsia with some degree of macula sparing.
● Visual agnosia: ( Impairment in recognizing visually presented objects,despite otherwise normal visual feild, acuity , color vision, brightness discrimination, language and memory)
● Prosopagnosia: ( Difficulty naming people on sight).
● Dyslexia: ( Difficulty reading) without agraphia ( Difficulty writing) ,color naming ( Anomia) ,and color discrimination problems.
● Memory defect .
● Topographic disorientation.
CENTRAL TERRITORY:
● Central post_ stroke ( thalamic) pain spontaneous pain and dysesthesias; sensory impairments.
● Involuntary movements; choreoathetosis, intention tremor, hemiballismus.
● Contralateral hemiplegia.
● Weber’s syndrome oculomotor nerve palsy and contralateral hemiplegia.
● Paresis of vertical eye movements, slight miosis and ptosis, and Sluggish pupillary light response.
Vertebrobasilar Artery Syndrome
● The vertebral arteries arise from the subclavian arteries and travel into the brain along the medulla where they merge at the inferior border of the Pons to form the basilar artery.
● The vertebral arteries supply the cerebellum ( via posterior inferior cerebellar arteries) & medulla ( via the medullary arteries).
● The basilar artery supplies the Pons ( via pontine arteries), the internal ear ( via labyrinthine arteries) & the cerebellum ( via the anterior inferior & superior cerebellar arteries ).
● Locked_ in syndrome ( LIS) occurs with basilar artery Thrombosis and Bilateral infarction of the ventral Pons. LIS is a catastrophic event with Sudden onset.
● Patients develop acute hemiparesis rapidly progressing to tetraplegia and lower bulwark paralysis ( CNs V through ×ll are involved).
● Initially the patient is dysarthric and dysphagia but rapidly progresses to mutism ( anarthria).
SIGNS AND SYMPTOMS:
Medial medullary syndrome:
● Ipsilateral to lesion paralysis with atrophy of half the tongue with deviation to the paralyzed side when tongue is protruded.
● Contralateral to lesion paralysis of UE & LE.
● Impaired tactile and proprioceptive sense
Lateral medullary ( wllenburg’s ) syndrome:
● Ipsilateral to lesion decreased pain and temperature sensation in face.
● Cerebellum or inferior cerebellar peduncle.
● Vertigo, nausea, vomiting.
● Nystagmus.
Horner’s syndrome:
● Miosis, ptosis, decreased sweating .
● Dysphagia and dysphonia: paralysis of palatial and laryngeal muscles , diminished gag reflex.
● Sensory impairments of Ipsilateral UE, trunk ,or LE.
● Contralateral to lesion impaired pain and thermal sense over 50% of body, sometimes face .
Complete basilar artery syndrome ( locked_ in syndrome):
● Tetraplegia ( quadriplegia).
● Bilateral cranial nerve palsy: upward gaze is spared.
● Coma.
● Cognition is spared.
Medial inferior pontine syndrome:
● Ipsilateral to lesion paralysis of conjugate gaze to side of lesion ( preservation of convergence).
● Nystagmus.
● Ataxia of limbs and gait.
● Diploma on lateral gaze.
Lateral inferior pontine syndrome:
● Ipsilateral to lesion horizontal and vertical nystagmus, vertigo , nausea, vomiting .
● Facial paralysis.
● Paralysis of conjugate gaze to side of lesion.
● Deafness.
● Ataxia.
● Impaired sensation over face.
Medial midpontine syndrome:
● Ipsilateral to lesion ataxia of limbs and gait ( more prominent in bilateral involvement).
● Contralateral to lesion paralysis of face ,UE,and LE.
● Deviation of eyes.
Lateral midpontine syndrome:
● Ipsilateral to lesion ataxia of limbs.
● Paralysis of muscles of mastication.
● Impaired sensation over side of face.
Medial superior pontine syndrome:
● Cerebellar ataxia .
● Internuclear opthalmoplegia.
Lateral superior pontine syndrome:
● Dizziness, nausea, vomiting.
● Horizontal nystagmus.
● Paresis of conjugate gaze ( Ipsilateral).
NEUROLOGICAL COMPLICATIONS:
Altered Conciousness:
Altered level of consciousness ( coma, decreased aurosal levels) may occur with extensive brain damage(e.g. large proximal MCA occlusion).
Disorders of Speech and Language:
Aphasia is the general term used to describe an acquired communication disorder caused by brain damage and is characterized by an impairment of language comprehension , and formulation and use.
In fluent aphasia ( wernicke’s / sensory / receptive aphasia), speech flowes smoothly with a variety of grammatical constructions and preserved melody of speech.
In non fluent aphasia ( Broca’s/ expressive aphasia), the flow of speech is slow and hesitant, vocabulary is limited, and syntaxes is impaired.
Global aphasia is a severe aphasia characterized by marked impairments of both production and comprehension of language. It is often an indication of extensive brain damage.
Receptive language functions ( auditory comprehension, reading comprehension) and expressive language function ( word finding, fluency, writing)
Dysphagia:
Dysphagia , an inability to swallow or difficulty in swallowing , occurs in about 51% of patients with stroke.
The most common problems seen in patients with dysphagia include:
Delayed triggering of the swallowing reflex
Reduced pharyngitis peristalsis
Reduced lingual control
Altered mental status
Altered sensation
Poor jaw and lip closure
Impaired head control, and poor sitting posture.
Cognitive Dysfunction:
Cognitive dysfunction may be present with lesions involving the cortex and includes impairments in alertness, attention orientation, memory, or executive functions.
Attention is the ability to select and attend to a specific stimulus while simultaneously suppressing extraneous stimuli.
Attention disorders include impairments in sustained attention, selective attention, divided attention, or alternating attention.
Altered attention results from lesions in the prefrontal cortex and reticulated formation.
Memory is defined as the ability to store experiences and perceptions for later recall. Immediate and long_ term Memory impairments are common , occurring in about 36% of patients with stroke.
Short_ term Memory loss is associated with lesions of the limbic system, limbic association cortex( orbitofrontal areas), or temporal lobes.
Long_ term Memory loss is associated with lesions s of the hippocampus of the limbic system.
Multi_ infarction dementia( vascular dementia) results from multiple small infarction of the brain and us seen in 6% to 32% of patients. It is more common in individuals over age 60 and is associated with episodes of Cerebral ischemia ( microvascular or small vessel disease) and hypertension. The patient exhibits impairments in memory and cognition and may fluctuate between periods of impaired function and periods of improved function.
Altered Emotional Status:
Lesions of the brain affecting the frontal lobe, hypothalamus, and limbic system can produce a number of emotional changes.
The patient with stroke may demonstrate pseudobulbar affect( PBA) also known as emotional liability or emotional dystegulation syndrome.
Depression is common occurring in approximately 35% of stroke cases. It is characterized by persistent feelings of sadness accompanied by feelings of hopelessness, worthlessness, and / or helplessness.
Depressed patients may also experience a loss of energy or persistent fatigue, an inability to concentrate, and decreased interest in daily life along with changes in weight and sleep patterns , generalized anxiety and recurrent thoughts of death or suicide.
