Case 4 – Headache & Progressive Hemiparesis

PC72 yo malec/o progressive r sided weakness over 2 weeksHPC2 weeks prior tripped and fell while playing tennisNo LOC and no associated injuriesThen developed difficulties using L upper extremity and weakness in L legAlso headaches increasing in frequency and intensityPMHx: BPH, MelanomaPSHx: Resection of melanoma 5 yrs agoMeds: NoneAllergies: PenicillinSHx: Married with 4 adult children. Lives at home with wife, retired engineerSubstance: Cigarettes – nil, EtOH – glass of wine nightly

O/E-Afebrile, BP 136/85, HR 92, RR 16-Alert and oriented to person, place & time;  CNs intactHealing ecchymosis on the right forearm and thigh.Increased tone in the left upper extremity.  No associated muscle fasciculation or muscle wastingPronator drift is noted on the left side.Weakness (4/5) is noted in all motor groups of the left upper extremity.Reflexes are brisk and symmetric throughout the upper and lower extremities.  Extensor plantar response on the left.

Q1  Is the patient’s examination consistent with an upper or lower motor neuron lesion?

Upper Motor Neuron Lesion

LOWER Motor Neuron Lesion UPPER Motor Neuron Lesion

Flaccidity Spasticity

Hypotonia Hypertonia

Hyporeflexia Hyperreflexia + Babinski

Fasciculation No fasciculation

Q2  What is the patient’s differential diagnosis?

Upper motor neuron lesion + asymmetric weakness:- Stroke- Space Occupying Lesion due to:a. Traumab. Infection unlikely (afebrile)c. Tumord. Demyelinating disease Multiple Sclerosise. Congenital unlikely in 72 yrs oldf. Vascular anomalies causing haematoma

Q3 What investigations would you order?  Justify

CT ScanMRI Angiography

Q4 Describe the findings on CT head scan.

Interpreting Brain Scans:

1. Symmetry •Do the two hemispheres look exactly the same?•Is there swelling on one side which displaces the midline•Possibly due to:• Collection of blood outside the brain• Tumor• Abscess within the brain & surrounding edema

2. Focal abnormalities•Loss of normal tissue occurs in plaques of demyelination or infarct of ischemic stroke•Blood of intracerebral haemorrhage or tumor mass

CT scan of the head showing a thrombus occluding the stem of the left MCA (hyperdense MCA sign)

Plaques of MS

Tumor mass involving the anterior aspect of the left frontal lobe 

3. Cerebral ventrices hydrocephalus?

4. Abnormality outside the brain•Focal collections of blood in subdural or extradural hematomas or tumor of meninges or skull

Meningioma

Q5 Discuss the aetiology, clinical presentation and course, management and outcome of subdural haematoma.

Aetiology

•Damage to bridging veins•Connecting cerebral hemispheres to superior sagittal sinus•Displacement of brain after head trauma tear the veins•Elderly susceptible brain atrophy stretching of bridging veins + increased space for brain to move•Infants susceptible Bridging veins thin walled•Arterial rupture (cortical arteries) can also result in SDH (20-30% of cases) mostly in temporoparietal region (bridging vein rupture SDH were predominantly frontoparietal)•Low CSF pressure (eg. After lumbar puncture) also reduction of buoyancy of brain increased shearing of bridging veins

Development of Chronic SDH

• After SDH dural collagen synthesis induced + fibroblasts spread over inner surface of the dura to form thick outer membrane then a thinner inner membrane develops encapsulation of the clot. This occurs in approx 2 weeks

• Over time Chronic SDH liquefy to form hygroma. More than half of all SDH liquefy and enlarge rather than staying in size

• This can present risk of recurrent bleeding expand the hematoma. Also hygroma has high protein can draw water osmotically

Clinical Presentation

• Depend on the severity of injury and location

• Eg. With posterior possa SDH present with symptoms of increased ICP: headache, vomiting, anisocoria (unequal size of pupils), dysphagia, cranial nerve palsies, ataxia, nuchal rigidity.

• Cerebral hypoperfusion due to increased ICP also can cause cerebral infarction (esp in posterior fossa as PCA vulnerable to compression along edge of tentorium) Kluver Bucy syndrome (placidity + loss of fear and anger, aberrant sexual behaviour, increased appetite)

•Acute SDH: 1 – 2 days after onset

•Subacute SDH: 3-14 days after onset

•Chronic SDH: 15 or more days• Insidious symptoms of headaches, light headedness,

apathy, cognitive impairment, somnolence, seizures• Contralateral hemiparesis compression of cortex

underlying hematoma• Ipsilateral hemiparesis lateral displacement of midbrain

caused by hematoma compression of contralateral cerebral peduncle against free edge of tentorium

Prognosis

- SDH requiring surgery mortality rate 40-60%. If present with coma, mortality rate 57- 68%

Prognostic factors:•Associated intracranial and extracranial injuries•Age•Neurologic status as assessed by GCS•Hematoma thickness•Hematoma volume•Presence and degree of midline brain shift

Q6  Which tumours most commonly metastasise to the brain?   Which are the most likely to haemorrhage?

•Lung — 16 to 20 percent•Melanoma — 7 percent•Renal cell cancer — 7 to 10 percent•Breast cancer — 5 percent•Colorectal cancer — 1 to 2 percent

Brain metastases from melanoma, choriocarcinoma, thyroid carcinoma, and renal cell carcinoma have particularly high propensities for spontaneous hemorrhage [12], while brain metastases from other primary tumors (eg, lung, breast) generally do not bleed spontaneously

Source: Wikipedia

Naaah...just joking...source: uptodate.

And if we have time:

http://www.youtube.com/watch?v=gyg8tihdLLQ