2. PC 72 yo male c/o progressive r sided weakness over 2 weeks HPC 2 weeks prior tripped and fell while playing tennis No LOC and no associated injuries Then developed difficulties using L upper extremity and weakness in L leg Also headaches increasing in frequency and intensity PMHx: BPH, Melanoma PSHx: Resection of melanoma 5 yrs ago Meds: None Allergies: Penicillin SHx: Married with 4 adult children. Lives at home with wife, retired engineer Substance: Cigarettes – nil, EtOH – glass of wine nightly

3. O/E -Afebrile, BP 136/85, HR 92, RR 16 -Alert and oriented to person, place & time; CNs intact Healing ecchymosis on the right forearm and thigh. Increased tone in the left upper extremity. No associated muscle fasciculation or muscle wasting Pronator 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.

4. Q1 Is the patient’s examination consistent with an upper or lower motor neuron lesion? Upper Motor Neuron Lesion LOWER Motor Neuron LesionUPPER Motor Neuron Lesion FlacciditySpasticity HypotoniaHypertonia HyporeflexiaHyperreflexia + Babinski FasciculationNo fasciculation

5. Q2 What is the patient’s differential diagnosis? Upper motor neuron lesion + asymmetric weakness: - Stroke - Space Occupying Lesion due to: a. Trauma b. Infection  unlikely (afebrile) c. Tumor d. Demyelinating disease  Multiple Sclerosis e. Congenital  unlikely in 72 yrs old f. Vascular anomalies  causing haematoma

6. Q3 What investigations would you order? Justify CT Scan MRI Angiography

7. Q4 Describe the findings on CT head scan.

8. 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

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

10. Plaques of MS Tumor mass involving the anterior aspect of the left frontal lobe

12. 3. Cerebral ventrices  hydrocephalus?

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

14. 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

15. 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

16. 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)

17. 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

18. 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

19. 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 spontaneously12 Source: Wikipedia Naaah...just joking...source: uptodate.

20. And if we have time: http://www.youtube.com/watch?v=gyg8tihdLLQ