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Showing posts with label cerebro vascular accident. Show all posts
Showing posts with label cerebro vascular accident. Show all posts

Partial MCA syndrome

Partial  MCA syndromes occur due to the following

  • Cortical collateral blood flow 
  • Differing arterial configurations
  • Partial syndromes can also occur due to emboli that enter the proximal MCA without complete occlusion, occlude distal MCA branches, or fragment and move distally.

Partial syndromes due to embolic occlusion of a single branch results in 

  • Hand, or arm and hand, weakness alone (brachial syndrome)
  • Facial weakness with nonfluent (Broca) aphasia with or without arm weakness (frontal opercular syndrome).
  • A proximal superior division occlusion of dominant lobe- A combination of sensory disturbance , motor weakness,  nonfluent aphasia suggests that an embolus has occluded the proximal superior division and large portions of the frontal and parietal cortices is infarcted
  • Inferior division occlusion dominant hemisphere- a fluent (Wernicke’s) aphasia without weakness, the inferior division of the MCA that supply the posterior part (temporal cortex) of the dominant hemisphere is probably involved. Jargon speech and an inability to comprehend written and spoken language are prominent features. It is often accompanied by a contralateral, homonymous superior quadrantanopia. 
  • inferior division of the MCA in the nondominant hemisphere -Hemineglect or spatial agnosia without weakness indicates that the inferior division of the MCA in the nondominant hemisphere is involved.

Occlusion of a lenticulostriate vessel from MCA produces small-vessel (lacunar) stroke within the internal capsule. 
This will result in 

  • Pure motor stroke 
  • Sensory-motor stroke contralateral to the lesion. 
  • Ischemia within the genu of the internal capsule produce
  • Primarily facial weakness followed by arm then leg weakness as the ischemia extends posteriorly within the capsule. 
  • The contralateral hand may become ataxic and dysarthria will be prominent (clumsy hand, dysarthria lacunar syndrome). 
  • Lacunar infarction affecting the globus pallidus and putamen  has only few clinical signs such as parkinsonism and hemiballismus 

What is malignant MCA territory infarcts ?

Malignant MCA territory infarct can occur 
  • Due to an occlusion of the proximal MCA (M1 segment) and they are associated with an 80% mortality rate 
Occlusion at the origin of the MCA  produce 
  • Severe flaccid hemiparesis/hemiplegia
  • Contralateral homonymous heinianopia
  • Hemianesthesia
  • Conjugate gaze deviation
  • Pupillary dilatation,
  • Progressive decrease in the level of alertness 
Neurological deterioration may occur independent from raised intracranial pressure 
Global aphasia occurs if the left MCA is occluded. 
Occlusion of the right MCA produces left body neglect, and bilateral eyelid ptosis
Eyelid ptosis may be an early sign of herniation in large hemispheric infarcts and attributed to upper
brainstem involvement 

Structures involved in MCA stroke

1.Paralysis of the contralateral face, arm, and leg and sensory impairment over the same area (pinprick, cotton touch, vibration, position, two-point discrimination, stereognosis, tactile localization, barognosis, cutaneographia -Somatic motor area for face and arm and the fibers descending from the leg area to enter the corona radiata and corresponding somatic sensory system
2.Motor aphasia: Motor speech area of the dominant hemisphere

3.Conduction aphasia: Central speech area (parietal operculum)

Apractagnosia of the nondominant hemisphere, anosognosia, hemiasomatognosia
4.Loss of topographic memory is usually due to a nondominant lesion, occasionally to a dominant one
5.Homonymous hemianopia (often homonymous inferior quadrantanopia): Optic radiation deep to second temporal convolution
6.Paralysis of conjugate gaze to the opposite side: Frontal contraversive eye field or projecting fibers
7.Nondominant parietal lobe (area corresponding to speech area in dominant hemisphere) involvement produce 

  • Unilateral neglect
  • Agnosia for the left half of external space
  • Dressing apraxia
  • Constructional apraxia,
  • Distortion of visual coordinates
  • Inaccurate localization in the half field
  • Impaired ability to judge distance
  • Upside-down reading, visual illusions (e.g., it may appear that another person walks through a table)
8.Central, suprasylvian speech area and parietooccipital cortex of the dominant hemisphere produce the following defects
  • Central aphasia
  • Word deafness
  • Anomia
  • Jargon speech
  • Sensory agraphia
  • Acalculia, alexia, finger agnosia, right-left confusion ( Gerstmann syndrome)

    Middle Cerebral Artery (MCA) Syndrome

    The clinical picture vary depends on the site of occlusion and availability of collaterals.It is characterized by:
    • Contralateral hemiplegia affecting the face and arm more than the leg.
    • Contralateral hemianesthesia affecting the face and arm more then leg. There is also loss of cortical sense like stereognosis, discrimination and tactile extinction.
    • Contralateral homonymous hemianopia or inferior quadrantanopia.
    • Aphasia when dominant lobe is involved
    • Inattention, neglect, denial of illness and apractic syndromes mainly with nondominant hemispheric lesions.
    • Paresis and apraxia of conjugate gaze to the opposite side.
    • Alexia and agraphia (Left angular gyrus lesion)
    • Gerstmann'ssyndrome (Fingeragnosia, acalculia dysgraphia and right-left disorientation).Infarction in the nondominant hemisphere result in it
    Perioral and distal upper limb sensory dysfunction is called as cheiro-oral syndrome,may occur . 
    Ataxic hemiparesis with cheiro-oral syndrome is sometime seen contralateral posterior capsular infarction 
    Rarely, nondominant infarction may result in  an acute confusional state and acute agitated delirium with affective and autonomic excitement, delusions, and hallucinations .
    Lesions of either hemisphere may result in  contralateral homonymous hemianopia or contralateral homonymous inferior quadrantanopia.
    Cataleptic posturing in isolation from other manifestations of the catatonic syndrome is also mentioned in association with MCA territory infarction 

    Symptoms of main artery occlusion:
    • Coma at the  onset.
    • Contralateral hemiplegia affecting  face and arm more than leg
    • Contarlateral hemihyposthesia with cortical sensory loss in upperlimb. There is also loss of cortical sense like stereognosis, discrimination and tactile extinction.
    • Contralateral homonymous hemianopia.
    • Aphasia and agraphia in left sided lesions.
    Capsular Branch Occlusion: (Lenticulo striate artery)
    • Contralateral complete hemiplegia affecting the upper and lower limbs to the same extent
    • Contralateral hemihyposlhesia of subcortical type.
    • Contralateral hemianopia may occur.
    • No loss of consciousness or aphasia.
    Cortical branch occlusion
    Frontal Branches occlusion:
    • Facio-brachial monoplegia.
    • Motor aphasia and agraphia in left-sided lesions.
    Parietal vessel occlusion:
    • Cortical sensory loss in the upper limb.
    • Lower.quadrantic homonymous hemianopia
    • Sensory aphasia (alexia) and apraxia in left sided lesions.
    Temporal  vessel occlusion
    • Upper quadrantic homonymous hemianopia.
    • Sensory aphasia (auditory agnosia).

    Posterior cerebral artery syndromes

    • In 75% of cases, both PCAs arise from the bifurcation of the basilar artery
    • In 20%, one has its origin from the ipsilateral internal carotid artery via the posterior communicating artery
    • 5%  both originate from the respective ipsilateral internal carotid arteries 
    The precommunal or P1, segment of the true posterior cerebral artery is atretic in such cases.
    PCA syndromes usually result from atheroma formation or emboli that lodge at the top of the basilar artery; 
    posterior circulation disease may also be caused by dissection of either vertebral artery and fibromuscular dysplasia.

    Two clinical syndromes are observed with occlusion of the PCA
    P1 syndrome : midbrain, subthalamic, and thalamic signs, this is due to P1 segment of PCA or of its penetrating branches such as thalamogeniculate, Percheron, and posterior choroidal arteries
    P2 syndrome : cortical temporal and occipital lobe signs, due to occlusion of the P2 segment distal to the junction of the PCA with the posterior communicating artery.
    P1 syndromes 
    Infarction usually seen in the following areas
    • Ipsilateral subthalamus
    • Medial thalamus 
    • Ipsilateral cerebral peduncle
    • Midbrain 
    A third nerve palsy with contralateral ataxia (Claude’s syndrome)
    A third nerve palsy with contralateral hemiplegia (Weber’s syndrome) 
    Structure affected
    • The ataxia is due to involvement of the red nucleus or dentatorubrothalamic tract
    • The hemiplegia is localized to the cerebral peduncle 
    • If the subthalamic nucleus is involved, contralateral hemiballismus
    • Occlusion of the artery of Percheron produces the following deficit
    • Paresis of upward gaze and drowsiness
    Extensive infarction in the midbrain and subthalamus occurring with bilateral proximal PCA occlusion presents as
    • Coma
    • Unreactive pupils
    • Bilateral pyramidal signs,
    • Decerebrate rigidity.
    Occlusion of the penetrating branches of thalamic and thalamogeniculate arteries result in less extensive thalamic and thalamocapsular lacunar syndromes. 
    The thalamic Dejerine-Roussy syndrome consists of contralateral hemisensory loss followed later by an agonizing, searing or burning pain in the involved  areas. It is persistent and will responds poorly to analgesics. Anticonvulsants (carbamazepine or gabapentin) or tricyclic antidepressants may be beneficial in treating it.
    P2 syndrome
    P2 syndromes occlusion of the distal PCA produce infarction of the medial temporal and occipital lobes. 
    • Contralateral homonymous hemianopia with macula sparing is the common manifestation. Sometimes , only the upper quadrant of visual field is involved. 
    • If the visual association areas are spared and only the calcarine cortex is, the patient may be aware of visual defects. 
    • Medial temporal lobe and hippocampal involvement may cause an acute disturbance in memory, especially if it occurs in the dominant hemisphere. As the memory has bilateral representation the defect usually clears.
    • If the dominant hemisphere is affected and the infarct extends to affect the splenium of the corpus callosum, the patient sometimes demonstrate alexia without agraphia. 
    Visual agnosia for faces, objects, mathematical symbols, and colors and anomia with paraphasic errors (amnestic aphasia) are seen in this setting, this is seen even without callosal involvement. 
    Occlusion of the posterior cerebral artery can produce peduncular hallucinosis it is manifested as visual hallucinations of brightly colored scenes and objects.
    Bilateral infarction in the distal PCAs produces
    Cortical blindness (blindness with preserved pupillary light reaction). 
    Antons syndrome -The patient is often unaware of the blindness or he or she may  even deny it .it is called as Anton’s syndrome
    Tiny islands of vision may persist, and the patient may sometime report that vision fluctuates as images are captured in the preserved portions. 
    Rarely, only peripheral vision is lost and central vision is spared,which will result in “gun-barrel” vision. 
    Balints syndrome-Bilateral visual association area lesions may result in Balint’s syndrome , a disorder of the orderly visual scanning of the environment .It is due infarctions secondary to low flow in the “watershed” between the distal PCA and MCA territories, as occurs after cardiac arrest. 
    Patients may experience persistence of a visual image for several minutes despite gazing at another scene called as palinopsia 
    An inability to synthesize the whole of an image termed as asimultanagnosia. 
    Top of basilar artery
    Embolic occlusion of the top of the basilar artery can produce any or all of the central or peripheral territory symptoms. 
    The hallmark is the sudden onset of bilateral signs, including 
    • Ptosis
    • Pupillary asymmetry or lack of reaction to light
    • Somnolence

    Clinical presentation of Posterior Cerebral Artery (PCA) occlusion

    The clinical presentation varies with the site of occlusion and availability of collaterals. Partial syndromes are common,Symptoms depends on the vessel of occlusion
    • Hemisphere branch occlusion
    • Bilateral hemisphere branches occlusion 
    • Callosal branch occlusion
    • Penetrating branch to thalamus occlusion
    • Penetrating branch to midbrain occlusion
    A. Hemisphere branch occlusion :
    • Contralateral homonymous hemianopia with occasional macular sparing
    •  Visual and Color agnosia
    B. Bilateral hemisphere branches occlusion 
    • Bilateral homonymous hemianopia
    • Cerebral blindness - bilateral visual loss with normal pupillary reflexes and fundus
    • Apraxia for ocular movements
    • Agnosia for familiar faces (Prosopagnosia)
    • Agitated delirium (mesiotemporo-occipital lesion)
    • Anton syndrome or denial of blindness(parietal lobes involved)
    • Balint syndrome- optic ataxia, psychic paralysis of fixation, inability to look to the peripheral field and disturbance of visual attention.
    C. Callosal branch occlusion
    This affects the left occipital region and splenium of corpus callosus and results in Alexia without agraphia (agnostic alexia)
    D. Penetrating branch to thalamus occlusion
    1. Dejerine and Roussy's Syndrome :
    • Contralateral hemianesthesia.
    • Transient contralateral hemiparesis.
    • Dysesthesia on the affected side (Thalamic Pain)
    • Involuntary movements - Choreoathetosis, hemiballismus, etc. (Ventral posteromedial and postero - lateral nuclei are affected).
    2. Aphasia (Left pulvinar nuclei affected).
    3. Amnesia (Mesial Thalamoperforators affected)
    4. Akinetic mutism
    E. Penetrating branch to midbrain occlusion
    1. Ipsilateral oculomotor palsy with contralateral hemiplegia (Weber's Syndrome)
    2. Ipsilateral oculomotor palsy with contralateral cerebellar ataxia (Nothnagel Syndrome)
    3. Ipsilateral oculomotor palsy with contralateral ataxia and choreoathetosis (Benedikt's syndrome)
    4. Parinaud's syndrome
    • Supranuclear paralysis of elevation
    • Defective convergence
    • Convergence retraction nystagmus
    • Lid retraction (Collier’s sign)
    • Skew deviation
    • Light near dissociation
    5. Unilateral or bilateral Internuclear ophthalmoplegia
    6. Pseudoabducent palsy
    7. Peduncular hallucinations - often silent, mobile and colorful and frequently pleasurable
    8. Decerebrate rigidity, Locked-in syndrome and disturbances in consciousness.