 Carotid artery syndromes

o Occlussion of the CCA (<1% of cases of stroke)

o By atheromatous plaque
o Left side > right
o Internal carotid a. territory infarction
 Drowsy/ stuporous – ill-defined effect on the RAS
o Incomplete occlusion
 Cortical watershed – in between two occluded branches
 Internal/deep watershed
o ICA supplies the optic nerve and retina
 Transient monocular blindness (Amaursosis fugax)
 Risk of developing stroke; a warning sign  impending occlusion
 Middle cerebral artery stroke syndromes
o MCA supplies the lateral convexity, Broca’s area, lateral gaze, white matter of parietal
lobes, Brodmann area, angular and supramarginal gyrus, superior parts of temporal
lobe, insula, Wernicke’s, large part of caudate nucleus (review)
o MCA supplies Internal capsule, claustrum, putamen
o MCA Stem occlusion syndrome
 Total occlusion
 Contralateral hemiplegia
 Hemianesthesia
 Homonymous visual field deficit
 Variant
o Global aphasia: left hemisphere
o Anosognosia and amorphosynthesis
 Onset: drowsy
 Usually embolus > thrombus
o Striatocapsular infarction
 Aka lenticulostriae/perforating vessels of MCA
 Deep lesions (e.g. on corona radiata)
o MCA Branch syndromes
 Superior division
 Supply rolandic and prerolandic areas – motor control
o Contralateral sensorimotor deficit
 Face, arm> leg
 “brachiofacial or chierobrachial paralysis”
 Gerstmann syndrome – agraphia, acalculia, finger
agnosia, R/L disorientation
 Left-sided lesions: initial aphasia, predominantly
broca’s aphasia
o No impairment of awareness
 Inferior division
 Less frequent
 Embolism
 Left-sided lesions: Wernicke’s aphasia – speak very well but hindi
nakakaintindi (does not appear frustrated)
  Right/Left-sided lesions: Superior quadrantanopia (“pie in the sky”)
orhomonymous hemianopia
 Anterior cerebral artery syndromes
o Recurrent artery of Heubner (largest of all deep branches of ACA/penetrating branches)
 Shares territory with mca
 Stroke causes infarction in head of caudate
 Affected in strokes d/t syphilis
 Usually affects the anterior limb of the internal capsule and caudate
 Arm paralysis, dysarthric, abulic, agitated
o Left-sided lesions: sympathetic apraxia of the same side or alien hand syndrome
o Sensorimotor deficit
 Contralateral foot and leg
o Mild or absent discriminative sensory loss
o Head and eye deviation
o Urinary incontinence
o Contralateral grasp reflex
o Paratonic rigidity (Gegenhalten)
o Language disturbances: transcortical motor aphasia (parang improving Broca’s aphasia)
o Disorder of behavior: abulia, slowness, muteness and distractability, mood changes
 Anterior choroidal artery syndromes
o Contralateral hemiplegia
o Hemihyopesthesia
o Homonymous sectorial hemianopia
o Embolic
o Right-sided: left-spatial neglect, constructional apraxia
 Posterior cerebral artery (PCA) syndromes
o 70% of individuals - from bifurcation of basilar artery (normal variant)
o Supply occipital lobe
o Proximal parts
 Interpeduncular
 Thalamoperforant, tghalaomegniculate
o Cortical parts– inferior temporal and medial occipital
o Dejerine roussy syndrome – thalamic infarcts: occlusion of thalamogeniculate branches
 Present with contralateral severe sensory loss, severe pain
 Give pregabalin, gabapentine, valproic acid, carbamazepine
o Central and Midbrain subthalamic syndromes
 Percheron vessel – supplies both sides of posteromedial thalamus
 Present with vertical gaze (sunset eyes/ nakatingin sa baba)
 Stupor/coma
o Paramedian artery syndromes/ midbrain syndrome
 3rd nerve palsy ipsilateral
 Weber syndrome – 3rd nerve palsy with contralateral hemiplegia
 Claude syndrome – 3rd nerve palsy with ataxic tremor
 Benedict syndrome – 3rd nerve palsy with contralateral ataxia and hemiplegia
(combined)
 Vertebral artery stroke syndromes
 o Chief arteries of medulla, lower ¾ of pyramid (motor), middle lemniscus (sensory),
posterior and inferior cerebellar arteries
o With 4 divisions
 V1 – from entry to cervical transverse foramen
 V2 - to uppermost foramen (c1 level)
 V3 – to dural penetration (near formen magnum)
 V4 – from foramen magnum until it becomes basilar artery
o Subjected to spondylothic compression, trauma
o Lateral medullary syndrome (Wallenberg) –


 Basilar artery syndrome
o Transient LOC
o Oculomotor disturbance
o Hemianopia
o Bilateral ptosis
o Pupillary enlargement with intact reactivity
 Lacunar stroke syndromes
o Very small diameter arteries
o Pure motor hemiplegia
o Pure sensory stroke
o Clumsy hand-dysarthria
o Ipsilateral hemiparesis-ataxia
 Treatment of ischemic stroke (Primary and secondary prevention)
o Acute phase management
 IV thrombolysis
 w/n 3-4.5 hrs of stroke onset
 eligibility criteria
o acute ischemic stroke
o 18 to 80 yrs
 Tissue plasminogen activators
o Converts plasminogen to plasmin
o Alteplase
o Tenecteplase: higher fibrin specificity and longer DOA
 o Dose 0.9 Mg/kg – 10 mg as initial bolus
 Followed by infusion of remainder for 1 hr
 Not exceed 90 mg
o 6% risk of symptomatic cerebral hemorrhage
 Endovascular thrombectomy or thrombolysis
 Large vessel occlusion
 Distal ICA or proximal MCA
 Can be done >4.5 hrs of stroke onset (until 24 hrs)
 Main criteria
o Occlusion of intracranial ICA or ACA
o Mismatch between the extent of stroke deficit and the volume
of ischemic but not yet infarcted tissue, as judged either
clinically or by imaging criteria
 Hemicraniectomy
 To reduce mass effect/edema/Increased ICP
o Medical management after stroke
 Acute stroke unit
 Prevention of venous thrombosis, pulmonary embolism, and coronary
syndromes
 Maintenance of normal BP: deferred to salvage the penumbra
 Maintenance of euglycemia
 Hydration: NO to any D5-containing fluids (glucose aggravates edema)
 Primary prevention
 Anticoagulants: AF patients
o Warfarin, rivaroxaban, dabigatran, Apixaban
 Antiplatelet drugs : not AF patients
o Aspirin, clopidogrel, ticlopidine, cilastazol
o ASA + clopidogrel in TIA for 21 days (CHANCE trial)
 HMG-CoA reductase inhibitors (statins) for secondary stroke prevention
o Advise lowering LDL to <70 mg/dl
o Reduce incidence of atherothrombosis;
 Physical Therapy and rehabilitation
 Less Common causes of Ischemic CVD
o Moyamoya disease
 Japanese term for “haze”/ “puff of smoke”
 Extensive basal cerebral rete mirabile
 A network of small anastomotic vessels at base of brain, around and
distal to circle of willis
 Segment stenosis or occlusiomn of the terminal intracranial parts of both ICA
 Associated with Down syndrome, certain HLA types (hereditary basis)
 Symptoms In young: Headache, convulsions, impaired mental clarity,
nystagmus, visual disturbances
 Symptoms In older: subarachnoid hemorrhage
 Strokes in children and young adults
 Intracerebral Hemorrhage
o 3rd most common cause of stroke
o Ruptured aneurysms, vascular malformations use of anticoagulants
 o Primary intracerebral hemorrhage (HICH)
 Putamen and adjacent internal capsule: 50%
 Lobar hemorrhages> Thalamus> cerebellar hemisphere> pons
 Sudden, in hypertensives (long term/uncontrolled  segmental lipohyalosis)
 Clinical syndrome: headache, acute hypertension, vomiting, hemiplegia
o Treatment of cerebral hemorrhage
 Adequate ventilation
 Acute use of controlled hyperventilation to PCO2 of 25-30 mmHg
 Monitoring of ICP
 Edema control (use of mannitol; if with ckd give hypertonic saline)
 IV infusion using saline solution
 Surgical evacuation/hemicraniectomy
 Spontaneous subarachnoid hemorrhage (SAH) and ruptured saccular aneurysm
o 4th most common frequent CVD
o Aneurysm common sites
 Proximal portions of anterior communicating ar.
 Origin of the posterior communicating a. from the stems of the internal carotid
 First major bifurcation of the middle cerebral artery
 Bifurcationof the internal carotid into the middle and anterior cerebral arteries
o SAH: clinical
 3 patterns
 Excruciating generalized headache, vomiting, LOC
o Worst headache of their life
 Severe headache, no LOC, stiff neck – most common
 Loss of consciousness, comatose
 Massive hemorrhage: sudden death
 Diagnosis - CT scan: blood in subarachnoid spaces, within brain, w/n ventricular
system
 Lumbar puncture
 Those not apparent on imaging studies
 Bloody tap (three successive bloody fluid samples)
 Increased opening and closing pressures (250-500 MM H2O)
 Digital subtraction angiography (DSA) – most sensitive
 CT and MRI angiography – usually requested
 SAH complications
 Rebleeding, vasospasm, hydrocephalus
 Treatment
 Bed rest
 Fluid administration
 Elastic stockings
 Stool softeners
 Nimodipine 60mg Q4
o Reduces incidence of stroke from vasospasm
 SBP of </= 150 mmHg
 Pain meds
 Arteriovenous malformations
o Tangle of dilated vessels that form an abnormal communication between the arterial
and venous systems
o Developmental abnormality
o Usually on Cortex or cerebral white matter
o Ruptured  mimics stroke
o Clinical and diagnostics:
 10-30 yrs old
 Intracerebral bleeding
 Seizures
 Bleeding risk of 3% per year
 CT or MR angiogram
o Treatment:
 Surgical excision
 Stereotactic radiosurgery (gamma knife)
 Endovascular embolization
 No treatment if small/not cortical/nonprogressive/asymptomatic