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Showing posts with label cerebrovascular accident. Show all posts
Showing posts with label cerebrovascular 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).

    The vertebral artery

    The vertebral artery arises from the following vessels
      Innominate artery on the right
     Subclavian artery on the left

         Segments of vertebral artery
    Vertebral artery has four segments
    The first (V1) -extends from its origin to its entrance into the sixth or fifth transverse vertebral foramen.
    The second segment (V2) -traverses the vertebral foramina from C6 to C2.
    ·    The third segment (V3) -passes through the transverse foramen and circles around the arch of the  atlas to pierce the dura at the foramen magnum.
    ·   The fourth segment (V4) -segment courses upward to join the other vertebral artery to form the  basilar artery; Only the fourth segment gives rise to branches that perfuse the brainstem and cerebellum
          Course of verebral artery
    Each vertebral artery passes upwards through the vertebral foramina to enter the cranial cavity through the foramen magnum and runs upwards on each side of the medulla. Both arteries meet at the lower border of the pons to form one midline single artery, the basilar artery, which runs upwards on the ventral surface of the pons were it gives small branches known as the paramedian arteries to the brain stem and divides into its two terminal branches the posterior cerebral arteries. Each posterior cerebral artery supplies the whole occipital lobe and the posterior part of the temporal lobe (posterior 2/5 of the cerebral hemisphere).
    Branches of vertebral artery
    In its course the vcrtebro-basilar system gives:
    Two spinal arteries which unit to form the anterior spinal artery.
    Three cerebellar arteries on each side. The superior middle and inferior cerebellar arteries.

    Etiology of VBI
    ·       Atherothrombotic lesions have a predilection for V1 and V4 segments of the vertebral artery.
    ·  Atheromatous disease rarely narrows the second and third segments of the vertebral artery, thisregion is prone  to dissection, fibromuscular dysplasia, and, rarely, encroachment by osteophytic spurs situated within the vertebral foramina.
    Clinical features of VBI
    The first segment may become diseased at the origin of the vessel and it produce posterior circulation emboli; If there is sufficient  collateral flow from the contralateral vertebral artery or the ascending cervical, thyrocervical, or occipital arteries it is usually sufficient to prevent low-flow TIAs or stroke.
    When one vertebral artery is atretic and an atherothrombotic lesion threatens the origin of the other, the collateral circulation, which may also include retrograde flow down the basilar artery, is often insufficient. This will promote, low-flow TIAs
    This state also sets the stage for thrombosis.
    Disease of the distal fourth segment of the vertebral artery can promote thrombus formation it will manifest as embolism or with propagation as basilar artery thrombosis.
    Stenosis occurring proximal to the origin of the PICA can threaten the lateral medulla and posterior inferior surface of the cerebellum.
    Embolic occlusion or thrombosis of a V4 segment causes ischemia of the lateral medulla.
    What is “subclavian steal.”?
    If the subclavian artery is occluded proximal to the origin of the vertebral artery this will result in reversal in the direction of blood flow in the ipsilateral vertebral artery. Exercise of the ipsilateral arm may result in  increase demand on vertebral flow, producing posterior circulation TIAs, or “subclavian steal.”
    Clinical manifestations of Vertebrobasilar insufficiency
    Clinicalfeatures of VBI consist of syncope, vertigo, and alternating hemiplegia
    Hemiparesis is not a feature of vertebral artery occlusion, however, quadriparesis may result from occlusion of the anterior spinal artery.

    Symptoms of Posterior cerebral artery infarct

    Origin of Posterior cerebral artery
    • The two PCAs are the terminal branches of the basilar artery in majority of people
    • In 20%—25% one of the posterior cerebral artery (PCAs) may originate from the internal carotid artery (ICA) via a posterior communicating artery
    The clinical presentation of PCA territory infarction is determined by the  
    • Site of occlusion 
    • Availability of collaterals. 
    1.Occlusion of the precommunal PI segment results in midbrain, thalamic, and hemispheric infarction.
    2.Occlusion of the PCA in the proximal ambient segment before branching in the thalamogenictulate pedicle results in lateral thalamic and hemispheral symptoms 
    3.Sometimes the occlusions may affect a single PCA branch, primarily the calcarine artery cause a large hemispheric infarction of the PCA territory.
    Causes of PCA infarct
    PCA infarct may be due to
    • Embolic
    • Thrombotic
    • Migrainous
    • Intrinsic atherosclerotic disease
    • PCA infarcts can also occur  due to compression of the artery against the tentorium during uncal herniation
    Whether embolic, thrombotic, migrainous, or due to intrinsic atherosclerotic disease, partial syndromes of the PCA are the rule
    1.Visualfield defect in PCA infarct
    1.Infarction in the distribution of the hemispheric branches of the PCA may cause a contralateral homonymous hemianopia
    This is due to infarction of
    • Striate cortex
    • Optic radiations
    • Lateral geniculate body
    There is partial or complete macular sparing if the infarction does not reach the occipital pole.
    2.The visualfield defect may be sometimes limited to a quadrantanopia. 
    A superior quadrantanopia is due to infarction of the striate cortex inferior to the calcarine fissure or due to involvement of the inferior optic radiations present  in the temporo-occipital lobes.
    An inferior quadrantanopia is the caused by an infarction of the striate cortex superior to the calcarine fissure or due to the superior optic radiations in the parietooccipital lobes
    3.Complex visual changes observed in  PCA infarct are 
    • Formed or unformed visual hallucinations
    • visual and color agnosias 
    • Prosopagnosia.
    Right hemispheric PCA infarctions may result in cause contralateral visual field neglect
    2.Sensory findings in PCA infarct
    Some alteration of sensation are also observed in PCA infarct
    They  are paresthesiae, or altered position, pain, and temperature sensations
    Sensors findings are due to thalamic ischemia  as a result of occlusion  of the precommunal or proximal postcommnual segments of the PCA
    Thalamoparietal ischemia due to occlusion of the more distal PCA or its parieto-occipital branches
    Brainstem ischemia is caused by vasoocclusive disease in the proximal vertebrobasilar arterial system
    3.Alexia without agraphia (pure word blindness)
    Infarction in the area of distribution of the callosal branches of the Posterior cerebral artery (PCA) tha affect  the left occipital region and the splenium of the corpus callosum results in alexia without agraphia (pure word blindness), occasionally this is associated with color anomia and object and photographic anomia .
    In this syndrome, patients is able to write, speak, and spell normally but are they are unable to read words and sentences. The ability to name letters and numbers is intact, but there may be inability to name colors, objects, and photographs.
     .4.Behavioural disturbance in PCA infarct
    Agitated delirium is seen with unilateral or bilateral penetrating mesiotemporal infarctions .
    Large infarctions in the left posterior temporal artery territory may produce an anomic or transcortical sensory aphasia
    Infarctions in the area of distribution of the penetrating branches of the PCA to the thalamus can result in aphasia
    If the left pulvinar is involved, akinetic mutism, global amnesia, and the Dejerine-Roussy syndrome can be seen
    5.Occlusion of calcarine artery
    Occlusion of calcarine artery may be associated with pain in the ipsilateral eye .
    Bilateral infarctions in the area of distribution of the PCA may result in bilateral homonymous hemianopia.
    Anton’s syndrome
    Bilateral occipital or occipitoparietal infarctions may cause  cortical blindness with preserved pupillary reflexes. Patients often deny or unaware of their blindness this is called as Anton’s syndrome.
    Bilateral altitudinal visual held defects rarely result from bilateral occipital lobe infarcts
    Infarction in the territory of the hemispheric branches of the PCA may also be accompanied by formed or unformed visual hallucinations called as release hallucinations ,
    Visual and color agnosias
    Prosopagnosia (agnosia for familiar faces). 
    Apraxia of ocular movements is often present with bilateral lesions.
    Balints syndrome
    Some patients with bilateral occipital or parietooccipital infarctions present with  Balints syndrome.
    Some patient with Proximal PCA occlusion may simulate MCA occlusion when it result in
    • Hemiparesis
    • Hemianopsia
    • Hemispatial neglect
    • Aphasia
    • Sensory  inattention .
    Cortical signs are probably explained by thalamic involvement

    Structures affected in PCA syndromes

    Symptoms and signs of stroke depends on the areas of brain affected and the stuctures involved .The various structures involved in central and peripheral territory stroke is given below
    Peripheral territory infarction
    • Homonymous hemianopia (often upper quadrantic): Calcarine cortex or optic radiation nearby.
    • Bilateral homonymous hemianopia, cortical blindness, awareness or denial of blindness; tactile naming, achromatopia (color blindness), failure to see to-and-fro movements, inability to perceive objects not centrally located, apraxia of ocular movements, inability to count or enumerate objects, tendency to run into things that the patient sees and tries to avoid-Bilateral occipital lobe with possibly the parietal lobe involved. 
    • Verbal dyslexia without agraphia, color anomia: Dominant calcarine lesion and posterior part of corpus callosum.
    • Memory defect: Hippocampal lesion bilaterally or on the dominant side only.
    • Topographic disorientation and prosopagnosia: Usually with lesions of nondominant, calcarine, and lingual gyrus.
    • Simultanagnosia, hemivisual neglect: Dominant visual cortex, contralateral hemisphere. 
    • Unformed visual hallucinations, peduncular hallucinosis, metamorphopsia, teleopsia, illusory visual pread, palinopsia, distortion of outlines, central photophobia: Calcarine cortex.
    • Complex hallucinations: Usually nondominant hemisphere.
    Central territory infarction
    • Thalamic syndrome: sensory loss (all modalities), spontaneous pain and dysesthesias, choreoathetosis, intention tremor, spasms of hand, mild hemiparesis: Posteroventral nucleus of thalamus; involvement of the adjacent subthalamic body or its afferent tracts. 
    • Thalamoperforate syndrome: crossed cerebellar ataxia with ipsilateral third nerve palsy (Claude’s syndrome): Dentatothalamic tract and issuing third nerve
    • Weber’s syndrome: third nerve palsy and contralateral hemiplegia: Third nerve and cerebral peduncle.
    • Contralateral hemiplegia:  Cerebral peduncle
    • Paralysis or paresis of vertical eye movement, skew deviation, sluggish pupillary responses to light, slight miosis and ptosis (retraction nystagmus and “tucking” of the eyelids may be associated):Supranuclear fibers to third nerve,interstitial nucleus of Cajal, nucleus of Darkschewitsch, and posterior commissure.
    • Contralateral rhythmic, ataxic action tremor; rhythmic postural or “holding” tremor (rubral tremor): Dentatothalamic tract.