stroke clinical manifestation

STROKE CLINICAL MANIFESTATION

- NITHIN NAIR

CLINICAL MANIFESTATIONThe focal neurological deficit resulting from a

stroke, whether embolic, thrombotic, or hemorrhagic, is a reflection of size and location of the lesion and the amount of collateral blood flow.

Clinical syndromes resulting from occlusion or haemorrhage in the cerebral circulation vary from partial to complete.

Ischemic stroke account for (80%), hemorrhagic stroke account for (20%) of strokes.

Clinical picture.... THROMBOSIS TIA EMBOLISM

Uneven progressionOnset develops within minutes or hours or days (thrombus in evolution)60% occur during sleep- patient unaware of problem, rises and falls to floorNo headache or in mild formComorbid factors – hypertension, diabetes, or vascular diseases.

Linked to atherosclerotic thrombosis.Preceded or accompanied by strokeLast 2-30 minutes (less than 24 hours)Normal neurological findings between attacksIf transient symptoms persist on awakening, may indicate future stroke.

Occurs rapidlyThere are no warningsMCA infarct (common)Headache Often a manifestation of heart diseases, including atrial fibrillation and MIAs embolus passes through artery, client may have neurological defecits that resolve as embolus breaks and passes into small artery

Clinical picture.... HYPERTENSIVE HEMORRHAGE RUPTURED SACCULAR ANEURYSM

Severe headacheVomiting at onsetBlood pressure > 170/90 (normally essential hypertension)Abrupt onsetGradually evolves over hours or days according to speed of bleedingNo recurrence of bleedingRapid improvement (not usual as hemorrhaged blood absorbs slowly.)

Asymptomatic before rupture.With rupture, blood spills under high pressure into sub arachnoid space.Excruciating headache with/without loss of consciousnessDecerebrate rigidity with comaIf severe – persistent deep coma, respiratory arrest, circulatory collapse leading to death (within 5 min)If mild – consciousness regained within hours then confusion, amnesia, headache, stiff neck, drowsiness.

GENERAL SIGNS AND SYMPTOMS

• Sensory : Tingling, numbness or decreased sensation (cortical sensations) on the affected side of the body.

• Crossed anesthesia (Ipsilateral facial impairments with contralateral trunk and limb involvement.)

General signs and symptoms.....

• Weakness : Paresis (80-90%)• Unable to generate force to initiate and

control movement.• UE > LE (affection)• Distal muscles > Proximal muscles ( strength

deficits)• Selective loss of type II fast-twitch fibres and

increase in percentage of type I fibres.


• Motor : Immediately after the onset of stroke, there is a stage of cerebral shock with flaccidity and areflexia. Gradually replaced by development of spasticity, hyperreflexia and synergy pattern.Upper extremities Lower extremities

Shoulder Girdle : depressor and retractor

Pelvic girdle : Retractors

Shoulder : internal rotators and adductors

Hip : Extensors, adductor and internal Rotators

Elbow : Flexors Knee : Extensors

Wrist and Finger : Flexors Ankle and Toes : Plantor flexors and supinators

Forearm : Pronators


Flexion Synergy Extension Synergy

Scapular retraction/elevation or hyperextension.Shoulder abduction, external rotationElbow flexionForearm supinationWrist and finger flexion

Scapular protractionShoulder adduction, internal rotationElbow extensionForearm pronationWrist and finger flexion

Hip flexion, abduction, external rotationKnee flexionAnkle dorsiflexion, inversionToe dorsiflexion

Hip extension, adduction, internal rotationKnee extensionAnkle plantarflexion, inversionToe plantarflexion


• An inspection of the synergy components reveals that following muscles do no take part in either of the synergies.

• Latissimus dorsi• Teres major• Serratus anterior• Wrist and finger extensors• Ankle evertors


• Reflexes : Flaccidity all reflexes are suppressed or absent.

• Spasticity Deep tendon reflexes become hyperactive, presence of clonus, plantar reflexes show babinski sign positive

• Release of primitive reflexes : ATNR (most common)• Associated reactions : Tonic postural reactions in

muscle. For eg: Vigorous contraction of elbow flexors (stronger UE) Flexion of hemiparetic elbow


• Altered Co-ordination : Proprioceptive losses sensory ataxia.

• Strokes affecting cerebellum cerebellar ataxia.

• Basal ganglia involvement bradykinesia or involuntary movements.


• Potural control and Balance: Reactive postural control and anticipatory postural control affected.

• Unable to maintain balance in sitting or standing or to move in a weightbearing posture without loss of balance.

• Disruptions in central sensorimotor processing.• Sitting /standing : asymmetry (weight shifted towards affected

side)• Postural sway in standing.• Delays in onset of motor activity, abnormal timing and

sequencing of muscle activity and abnormal co-contraction disorganization of postural synergies.


• Visual Changes: Homonymous hemianopia (loss of vision in the nasal half of one eye and temporal half of the eye corresponding to the hemiplegic side)

• Visual negelect (visual inattention)• Lack of conjugate gaze


• Speech and language changes : This occurs due to lesion involving dominant parietal lobe.

Broca’s/motor/expressive/non-fluent aphasia

Wernicke’s/sensory/receptive/fluent aphasia

Global/conductive /total aphasia

Ability to understand – intactAbility to respond – affectedDifficulty in articulating speech

Ability to understand – affectedAbiity to respond – intactSpeech is totally irrelevant

Loss of understanding and production of speechIndication of extensive brain damage.


• Apraxia : (Inability to carry out learned purposeful movements )

Ideomotor Ideational Constructional

Understands purpose of movementUnable to do it on commandDoes it automatically

Extreme absent-mindednessFails to perform purposeful movement both spontaneously and on command

Difficulty in spatial organisation of movement or objects.Inability to imitate.


• Agnosia : (Failure to recognise objects despite having an intact visual, auditory and tactile sensations) Visual Auditory Tactile

Inability to recognise common objects which is seen clearly by patient.Lesion in the dominant parieto-occipital region.

Inability to recognise familiar sounds or music.Lesion in the dominant temporal lobe.

Inability to recognise object by using hand although there is no sensory defect.Lesion in dominant parietal lobe.


• Perceptual Dysfunction : (Occurs due to lesion of non dominant parietal lobe)

• Body Scheme/ Body Image dysfunction : (Unilateral neglect, Anosognosia, Somatoagnosia, Right-left discrimination, Finger agnosia)

• Spatial relation disorder ( figure ground discrimination, form discrimination, topographic disorientation, vertical disorientation, depth and distance disorientation)


• Cognition and behavioral changes : (Occurs due to lesion of either of cerebral hemisphere)

• Left hemisphere lesion – depressed, low profile, anxious and have a negative attitude towards life, cautios and insecure

• Right hemisphere lesion – euphoric, over-confident, impulsive, over estimate their capacity, denial of being disabled.

• Difficulty in orientation, attention, conceptual abilities, memory and learning (short-term memory usually affected)


• Dysphagia : (occurs in patients with bilateral cerebral hemisphere or brain stem lesion

• Leading to – aspiration • Contibutors – altered sensation, incomplete

laryngeal elevation and closure, palatal paralysis, defective lip closure and postural imbalance.


• Bowel and bladder dysfunction: (Common in acute phase. In flaccid state – overflow incontinence. Disturbance in bowel functions – incontinence and diarrhoea or constipation and impaction.)

• Sexual dysfunction : Affects individual desire, libido, erectile or lubrication, orgasm or ejaculation. It could be due to depressed state or sensorimotor dysfunction.

Secondary manifestations

• Psychological dysfunction : Depression, social withdrawal, anxiety, insomnia, emotional liability, aggressiveness, verbal abusing, over dependancy)

• Deep Vein Thrombosis : ( occurs in hemiplegia due to immobilization)

• Cardiac and Respiratory deconditioning: occurs due to decreased physical activity. Endurance level is drastically reduced.

Secondary manifestations

• Pain : Common in stroke affecting thalamus ( thalamic syndrome). Intense burning pain on the opposite side of body.

• Musculoskeletal complications : Pain and joint stiffness (common), Subluxation of GH joint on affected side ( due to decreased tone in flaccid stage), loss of ROM and contractures, disuse atrophy, osteoporosis.

REFERENCE....PHYSICAL REHABILITATION –

SUSAN O’B SULLIVANNEUROLOGICAL

REHABILITATION – DARCY UMPHRED

PHYSIOTHERAPY IN NEURO CONDITIONS – GLADY SAMUEL RAJ

stroke clinical manifestation

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