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Showing posts with label stroke. Show all posts
Showing posts with label stroke. Show all posts

Antiplatelet agents for the treatment and prevention of atherothrombosis

Antiplatelet drug is a generic term, these are drugs used to decrease platelet aggregation and inhibit thrombus formation. They are most effective for arterial clots that are rich in platelets.

Platelets play crucial role in haemostasis and the development of arterial thrombi. Damaged endothelium activates platelets and they respond by adhering and aggregating. They release thromboxane A2 and adenosine diphosphate (ADP) that amplifies and propagates the process by stimulating surrounding platelets. The production of thrombin via the coagulation cascade is also accelerated, helps in stabilising the thrombus by the conversion of fibrinogen to fibrin. Different classes of antiplatelet drugs act at different junctures in this process.

Aspirin (ASA)

ASA is an antiplatelet agent widely used in the management of acute coronary syndromes (ACSs) and acute ischemic stroke. Other clinically useful effects of ASA are anti-inflammation and antioxidation. ASA is typically used alone or in combination with thienopyridines to manage ACSs or prevent stent thrombosis. This is an indirect thombaxane inhibitor,it irreversibly inhibits the platelet cyclooxygenase (COX)-1 enzyme. ASA, if given at low doses,specifically inhibits plateletsynthesis of thromboxane A2 and this will leads to antithrombotic effect. At medium doses aspirin inhibits both COX-1 and COX-2 by blocking the prostaglandin synthesis and it has analgesic and antipyretic effects.This is why ASA at high doses is effective as an anti-inflammatory drug in treating rheumatic disorders.
However, ASA is a weak inhibitor of platelet aggregation when compared to other antiplatelet medication so typically it is used in combination with other antiplatelet drugs. It is conveniently dosed for once a day and recommended to be taken with food to reduce the gastrointestinal side effects.

Clopidogrel is a thienopyridine ADP-receptor antagonist which irreversibly binds to the P2Y12 receptor.An ADP receptor antagonist that competitively inhibits ADP from binding to platelet receptors, preventing ADP-mediated up-regulation of glycoprotein (GP) IIb/IIIa receptor, again blocking amplification of platelet aggregation. Clopidogrel, is administered orally once a day, this may have variable responses and has a delayed onset of action from 2 to 6 hours if clopidogrel is given as a loading dose of 600 mg onset of action is 12 to 24 hours .There is chance of drug interaction if. used with proton-pump inhibitors (PPIs).
Clopidogrel is used alone in those who cannot tolerate aspirin prophylaxis.
Clopidogrel is routinely used in the treatment of acute coronary syndrome (ACS) and post-percutaneous coronary intervention (PCI) stenting in conjunction with aspirin.

Prasugrel is a prodrug from the same family as clopidogrel, with more efficient platelet inhibition, a thienopyridine that inhibits the ADP receptors on the platelets, hence preventing them from aggregating and causing blood clots. It will irreversibly binds to the P2Y12 receptor. Thienopyridine group of drugs are more potent than ASA.. Prasugrel is given by mouth once a day, beginning with a loading dose and followed with maintenance doses. Prasugrel is the newest thienopyridine drug and it does not have similar concerns of decreased efficacy in those patients who are poor metabolizers or are using concurrent PPIs.
Prasugrel is used in combination with aspirin in ACS patients undergoing primary PCI when:
Immediate PCI is necessary for ST-segment elevation myocardial infarction (STEMI); or
Stent thrombosis occurred during treatment with clopidogrel or
The patient has diabetes mellitus.
This combination is recommended for 12 months only - beyond which there is doubtful clinical benefit.

Dipyridamole act by inhibiting the activity of adenosine deaminase and phosphodiesterase, this will result in accumulation of adenosine, adenine nucleotides, and cyclic adenosine monophosphate. Dipyridamole further inhibits platelet aggregation and leads to vasodilation. This is usually used in ombination with other anticoagulants to prevent thromboembolic complications after surgery. The problem of using dipyridamle is inconvenience, because of multiple doses administered by mouth per day. Dipyridamole is also available in combination with ASA under the brand name Aggrenox and is used to derease the risk of stroke. Aggrenox is usually given by mouth twice daily.It is also used as a stress test agent.
Since Dipyridamole also has vasodilating properties this is unsuitable for use in those with severe coronary artery disease, unstable angina, recent myocardial infarction or left ventricular outflow obstruction

Ticlopidine is one of the first antiplatelet drugs available, is a platelet aggregation inhibitor and is usually used to reduce the risk of thrombotic stroke and administered by mouth two times a day. Ticlopidine was once routinely used but has been falling out of favor because of serious hematological side effect profiles 

Glycoprotein IIb/IIIa antagonists
These drugs inhibit the final common pathway of platelet aggregation where fibrinogen binds to GP IIb/IIIa receptor.Abciximab ,Eptifibatide,Tirofiban
All these drugs require intravenous administration under specialist supervision with close monitoring, usually on coronary care units (CCUs).
Thromboxane A2 and ADP are just two of over 90 known platelet agonists. Blockade by aspirin and clopidogrel will not affect the platelet's ability to be stimulated by other agonists while use of a GP IIb/IIIa antagonist should inhibit aggregate formation whatever agonist influences the platelet.
Since there is chance of neutralising antibodies to abciximab is formed  it can only be used once.
GP IIb/IIIa antagonists can cause severe bleeding, most common from the site of femoral puncture for percutaneous transluminal coronary angioplasty (PTCA). It may take over 12 hours for platelet function to be restored after stopping this infusion

This is licensed for use with aspirin in preventing atherothrombotic events in ACS for 12 months, and is recommended for use for both medical management or where further coronary intervention is planned.

Features of Anterior cerebral artery occlusion

Main Artery Occlusion:clinical features
  • Contralateral hemiplegia affecting Lowerlimb more than Upperlimb.
  • Contralateral cortical sensory loss in live lower limb.
  • Incontinence of urine.
  • Mentality and personality changes.
  • Forced grasp reflex.
Capsular branch occlusion (Heubner Artery) clinical features
  • Faciobrachial monoplegia which is proximal more than distal, i.e. involving the shoulder more than the hand.
Cortical Branches occlusion clinical features

Frontal vessel occlusion: clinical features
  • Mentality and personality changes.
  • Forced grasp reflex.
Paracentral vessel occlusion:
  • Monoplegia in the lower limb.
  • Cortical sensory loss in the lower limb.
  • Urinary incontinence.
Callosal vessel occlusion:
  • Apraxia of the left side.

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.

    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.

    Definition of stroke

    1.WHO definition
    A neurological deficit.
    Sudden onset.
    With focal rather than global dysfunction.
    In which, after adequate investigations, symptoms are presumed to be of non-traumatic vascular origin and last for > 24 hours

    2. NINDS 2005 (National Institute of Neurological Disorders and Stroke)
    When the blood supply to part of the brain is suddenly interrupted or when a blood vessel in the brain bursts.

    3.TIA (Transient Ischemic Attack)
    Neurological deficit of vascular origin lasts from few minutes to hours and resolves within 24 hours. 

    Inclusion and exclusion criteria for thrombolysis in strok

    Inclusion criteria
    Clinical  signs and symptoms of definite acute stroke
    Clear time of onset
    Presentation within 3 hrs of acute onset
    Haemorrhage excluded  by CT scan
    Age 18 - 80 years old 
    NIHSS less than 25
    Consent to treat (every effort must be made to contact next of kin)

    Exclusion criteria
    Rapidly improving or minor stroke symptoms
    Stroke or serious head injury 3 months
    Major surgery, obstetrical delivery, external heart massage last 14 days, 
    Seizure at onset of stroke
    Prior stroke and concomitant diabetes
    Severe haemorrhage last 21 days
    Increase bleeding risk
    History of central nervous damage (neoplasm, haemorrhage, aneurysm, spinal or intracranial surgery or haemorrhagic retinopathy)
    Blood pressure above 185 mmHg systolic or 110 mmHg diastolic
    Symptoms suggestive of SAH (even if CT is normal) 
    Known clotting disorder
    Patient on heparin or warfarin
    Suspected iron deficient anaemia or thrombocytopenia
    Suspected hypoglycaemia or hyper glycaemia >3 mmol/l > 22 mmol/l
    Bacterial endocarditis, pericarditis
    Acute pancreatitis
    Ulcerative GI disease last 3 months, oesophageal varices, arterial-aneurysm, arterial/venous malformation.
    Severe liver disease including cirrhosis, acute hepatitis