CVA

 

Etiology:

  1. Ischemic:
    1. aThrombosis in situ- atherosclerosis,
       
    2. Tromboembolic:     
      1. in artery - vasculitis, SLE, aneurysm, SS.
      2. cardiac origin -A.fib,  mitral / aortic valve disease, cardiomyopathy.
         
    3. TIA - transient ischemic attack that resolves in <24 hr., commonly in 1 hr.  TIAs are probably 2ry to  microemboli.
       
    4. Venous occlusion (sinus thrombosis), CAT and VAT  (Carotid and Vertebral Artery Dissection - see section on "Headache")
       
  2. Hemorrhagic:
    1. SDH-2ry to tearing of bridging veins (see "Head injury" in "Trauma" chapter
      )
    2. ICH -intracranial hemorrhage 2ry to HTN, vasculopathy
       
    3. SAH-2ry to aneurysm or AV malformation.
       

S & S: Depends on the etiology and area / artery involved.

  1. Ischemic:
     
    1. Middle cerebral Artery (MCA)
      • Upper extremities more affected than lower (hemiplegia)
         
      • One part of body has  sensory ; face, arm  or leg (hemisensory loss) - rarely loss of all  modalities
         
      • One part of body has  strength;  face, arm or leg (hemiparesis) - most apparent in distal extremities. If mild can be detectable as clumsiness of one hand or foot
         
      • Aphasia, almost always L hemisphere is affected
         
      • Left-side neglect with non-dominant R hemisphere involvement.
         
    2. Anterior  cerebral Artery (ACA)
       
      • Lower extremity  more affected than upper (hemiplegia)
         
      • Weakness and sensory loss in one leg
         
      • Urine incontinence
                                                                              
    3. Vertebral / Basilar Artery Insufficiency (VBI)
       
      • Ataxia / Dizziness / Nystagmus
         
      • N/V
         
      • Drop-like attack without LOC
         
      • Cerebellar signs (finger-nose, heal-shin), clumsiness
         
      • Coma (if midbrain and pons become involved by basilar artery)
         
    4. Posterior Cerebral Artery (PCA)
      • Cortical homonymous hemianopsia with spared central  vision.
         
      • Amnesia - sometimes
         
      • Dyslexia - sometimes
         
    5. Lacunar Infarcts  = common 4 syndromes are identified. These syndromes are not really anatomically specific - often result from lesions in internal capsule, basal ganglia, brainstem.
       
      • Pure motor hemiplegia = lesion in pons which  affects face, arm or leg.
         
      • Clumsy hand dysarthria = lesion of midpons
         
      • Pure sensory deficit = lesion in thalamus
         
      • Leg weakness and ataxia = lesion in pons
         
    6. Transient Global Amnesia (TGA)
       
      • Abrupt memory loss that can occur at any age. Risk factors are migraine in young. TIA was suggested as a possibility
         
      • Anterograde memory is affected and pt is unable to acquire  new information and remember anything for more than few minutes. Typically pt will ask the same question over and over (almost diagnostic!). Retrograde amnesia  of events occurring a few weeks to a few months prior, may  also occur.
         
      •  Physical activity, and complex skills remain intact while pt noted to act strange. Rest of neurological exam is intact. Some pts may experience N/V, HA.
         
      •   Complete recovery is seen in < 24 hr. Pts are sometimes treated with ASA although the real benefit is questionable since the pathogenesis doesn't appears to be related to atherosclerosis

          
  2. Hemorrhagic:
     
    1. Subarachnoid Hemorrhage (SAH)
      • Usually sudden and severe HA . If asked, pt may report it as "the worst HA of  my life", but many pt's  will describe a lot of pains and aches as "the worst…" making this statement very non specific.
         
      • Meningeal signs usually present
         
      • Possible Stupor / Coma /LOC
         
      • Papiledema or  fundal hemorrhage can be present
         
      • Generally no focal signs
         
    2. IC hemorrhage  (ICH) 
      1. Secondary to HTN, vasculopathy
         
      2. Often focal neural symptoms, with prominent  HA, N/V and drowsiness.
         
      3. Bradycardia, Tachypnea,  anisocoria (2ry to  IC pressure)
         
      4. The following S & S may help in locating the lesion:
         
        1. Putamen - conjugate deviation of eyes towards the lesion + signs of MCA.
           
        2. Thalamus - medial deviation of both eyes + hemisensory deficit
           
        3. Pons - pinpoint pupils and midline location  of eyes + coma and deficit of reflex (no ocular deviation).
           
        4. Cerebellum - inability to look towards the lesion side + N/V, ataxia, cerebellar signs, dizziness. This is a treatable entity if rapidly diagnosed.

Diagnosis:

  1. In addition to above symptoms one has to address Mini Mental Test, GCS, pupils, Doll's eyes, posture  (Decorticate = hemispheric insult or Decerebrate = midbrain or pons lesion), reflexes (Babinski) and muscle tone.
     
  2. CT of head. May not show infarct until 24 -48 hours.
     
  3. In case of SAH, sensitivity  of  CT decreases with time. Although MRI is superior to CT in detecting bleed, it is yet unclear sensitivity/specificity of  the MRI for SAH. If SAH is a concern, LP is done after CT. On LP one looks for xanthochromia. This develops after  6-8 hrs. from beginning of symptoms, but the presence of RBCs on LP is diagnostic for SAH. If RBCs gradually decrease from tube 1 4 LP is a traumatic tap.

Treatment:

  1. ABC are #1 priority. Airway must be established in pt that presents with CVA signs and  now has N/V, or decreased MS or absent gag reflex.
     
    1. Ischemic:
       
      • If no blood on CT, pts are generally anticoagulated with ASA (have neuro consult).
         
      • t-PA if stroke is <3hrs and CT is (-)ve. Consult neurologist prior to this approach.
         
      • BP shouldn't be lowered abruptly and preferably maintained >150 systolic. Although commonly practiced, no data to support  the lowering of BP in ischemic stroke
         
      • TIA can be treated with ASA and pt can be DC unless there is  no improvement of symptoms in less than 24 hrs (accelerating TIA) or recurrent symptoms (stuttering TIA) in which case pt admitted for anticoagulation.
         
    2. Hemorrhagic:
       
      1. SAH
        • Neurosurgical consult
           
        •  Maintain BP systolic 140-160mmHg
           
        •  Mannitol if edema and midline shift.
           
        •  CCB (nimodipine) decreases blood vessel spasm and useful if initiated within 72hrs.
           
      2. ICH
         
        • Neurosurgical consult
           
        • Since the etiology is HTN, it is common practice to lower BP by  20%. Yet, also in cases of  hemorrhagic stroke, no data exists  to support lowering BP.
           
        • If shift is present, Mannitol 1-1.5g/kg (70-100g) IV in < 30min and then  over next 23 hrs.
           
        • Elevate head > 30

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