Sem 2 Path Quiz

1. Sem 2 Path Quiz Neuro

2. Hydrocephalus Describe to flow of CSF. Where is it produced and where is it reabsorbed? What are the two types of hydrocepalus? Obstructive and Communicating (prob @ arachnoid granulations)

3. Congenital Malformations 1. Arnold Chiari malformation and Hydrocephalus (The abnormality in A C Malformation consists in elongation of the medulla and part of the cerebellartonsils into the foramen magnum. This causes compression of the central canal of the spinal cord with obstruction and resulting hydrocephalus.) Red arrows are a meningomyelocele (herniation of meninges through spinal column) 2. Syringomyelia. Which is? A fluid filled, cleft like cavity in the inner part of the spinal cord 3. Hydromyelia. Which is? Discontinuous expansion of the central canal of the spinal cord 4. Tuberose sclerosis is an autosomal dominant hereditary condition characterised by the development of harmatomas and benign neoplasmsinvolving brain and other tissues. 1 2 4 3

4. 2 1 Congenital Malformations 1. Porencephaly characterised by large (holes) cysts in the brain. 2. Lissencephaly. Abnormal development of the sulci and gyri 3. Down's syndrome. The antero-posterior shortening, with a steeply rising occipital contour (best seen side on) and overall rounding in shape, is characteristic. 4. Tay-Sachs disease. This is one of the hereditary lipid storage diseases and it results in mental deficiency. 3 4

5. Cerebral Palsy Gross cerebral atrophy in a man aged 45 with severe spastic diplegia ("cerebral palsy"). Note the thin gyri and how widely spaced they are.

6. Cerebral atrophy and severe atheromaof the cerebral arteries

7. Huntingtons Chorea Huntington's chorea. Marked atrophy of the basal ganglia is a characteristic feature of this condition, is well shown. This is a familial disease characterised by the onset of dementia at about the age of 40. The dementia is accompanied by choriformmovements. Degeneration of the striatal neurons What part of the basal ganglia are affected? Marked atrophy of the caudate nucleus

8. Alzheimer's disease cerebral atrophy What are the characteristic micro findings? Neuritic plaques (1) and neurofibrillory tangles (2). Rounded deposits of amyloidare usually present in the plaques and there is amyloid in the walls of blood vessels 3. Amyloid deposition in a blood vessel inAlzheimer'sdisease (Congo red stain) 2 1 3

9. Parkinsons Parkinson’s Disease is thought to be caused by? progressive loss of dopaminergic neurons in the basal ganglia. It presents as? ~50 as increasing slowness of movement, rigidity of muscles and tremor. There is also reduced emotional movement of the facial muscles giving a ‘mask like facies.’ The main abnormality seen in post mortem brains is? loss of pigment in the substantianigra. The lower specimen is from a normal brain for comparison. Microscopic examination of the substantianigrashows the presence of round, red staining inclusions in the neurons called Lewy bodies.

10. Multiple Sclerosis Multiple sclerosis is a demyelinatingdisease that affects mainly women from about 20 to 50 years of age. Presents as? Common presenting symptoms are sudden impairment of vision from an acute neuritis, or weakness of the lower limbs. Characteristically the symptoms disappear within days or weeks of their onset only to recur at a later time. There are many clearly defined, semitranslucent, glial plaques in the white matter. After the acute demyelinationthe plaques are surrounded by gliosis.

11. Meningitis See the purulent material filling the subarachnoid space. Patient is 3 months. What are the likely organisms? H.Influenzae, s.pneumoniae (Pneumococcal meningitis)

12. Acute Pyogenic Meningitis (pneumococcal) There is a copious purulent exudate in the subarachnoid space. Note also the very congested blood vessels. What would her CSF profile have been? Turbid colour, low Glucose, high protein, polymorphonuclear cells, Gram +

13. Tuberculous meningitis Note changes at base of brain, with adhesions present (arrows). The haemorrhage is probably the result of neurosurgical exploration.

14. Brain stem tuberculomas Tuberculomasare granulomatous masses that mimic the clinical and gross pathological features of a neoplasm.

15. Cryptococcal Meningitis What are the risk factors for infection with cryptococcus? AIDS, hodgkins lymphoma, sarcoidosis and long term corticosteroid therapy. This patient was a woman aged 66 with a thymomaand myasthenia gravis, who was treated with large doses of prednisone. Note characteristic opacificationof meninges.

16. cryptococcal meningitis Shows expansion of the subarachnoid space (arrows) by inflammatory cells. On higher power there are macrophages and some multinucleated giant cells (black arrow) indicating granulomatous meningitis. The cryptococciare visible as refractile bodies (red arrows) in the centres of empty spaces that occur because the mucin of the capsules of the organisms has been dissolved by the processing fluids. The organisms can be highlighted with mucin stains.

17. Cerebral Abscess What are the mechanisms of spread for brain abscess? Direct implantation, local extension, haematogenous spread This is a large acute streptococcal cerebral abscess The cavity is lined by necrotic brain tissue. The anterior horn (blue arrow) of the right lateral ventricle is also filled with pus. List 2 complications of brain abscess Herniation, rupture

18. Chronic cerebellar abscess

19. Herpes simplex encephalitis The main change is cerebral oedema with narrowing of sulci. Both parents had recently suffered from cold sores, and herpes simplex type I virus was grown from brain tissue taken at autopsy. Microscopy shows extensive neuronal necrosis, intranuclearacidophilic inclusions, and round cell infiltration with perivascular cuffing. Histology - Herpes encephalitis. In this case the perivascular cuffing by lymphocytes (arrows) is well seen, but intranuclear inclusions were not readily found in the neurones.

20. Creutzfeldt-Jakob disease At low power the grey matter contains clear spaces or vacuoles. These are usually not found in the white matter. At higher power the vacuoles (arrows) are seen more easily. Spongiform encephalopathy Prevalence? 1 in 1,000,000 How does it present? Rapidly progressive dementia How long will they survive? 7 years

21. Hydatid disease Note hydrocephalus and daughter cyst (red arrow) lying free in dilated ventricle.

22. Cysticercosis This disease is due to the infestation of man as an accidental intermediate host; Name the parasite tapeworm Taeniasolium.

23. Cerebral malaria This man is from PNG. What is the likely organism? Plasmodium falciparum. What do you see? the changes seen are due to plugging of the vessels by infected red cells with secondary hypoxia and small ring haemorrhages. (Note the similar appearance to that seen when fat embolism affects the brain.)

24. Brain tumours in children tend to be low grade astrocytomasor high grade medulloblastomas. Brain tumours in adults tend to be high grade astrocytomasor benign meningiomas. 20% of childhood cancers are brain tumours. Most brain tumours of childhood arise in the posterior cranial fossa. Most brain tumours in adults arise above the tentoriumcerebelli. The major complications of brain tumours are: Local (i) Loss of function (ii) Epilepsy (iii) Haemorrhage General (i) Raised intracranial pressure (ii) Herniation of brain

25. Multiple neurilemmomas (arrows) in a woman aged 23 with neurofibromatosis. There is a tumour on each vagus nerve, another in the wall of the oesophagus near the bifurcation of the trachea, and a fourth is applied to the anterior aspect of the left bronchus.

26. Histology of a Schwannoma Section shows spindle shaped Schwann cells with palisaded nuclei. These are tumours derived from Schwann cells which produce the myelin of myelinated peripheral nerve fibres (oligodendrocyteshave the same function within the central nervous system). They may occur within the cranial vault where they are often associated with the VIIIthcranial nerve (acoustic neuroma). Patients present with tinnitis and deafness. Other common sites are the dorsal roots of the spinal cord. MalignantSchwannomas arise de novo and not from benign Schwannomas.

27. Neurofibroma Types: Cutaneous Solitary Plexiform (cant separate from nerve) Rib with neurofibroma Gut with plexiformneurofibroma Histology of neurofibroma (Histology of neurofibroma (in skin). Note the 'squiggly' spindle shaped cells.) Familial syndromes Neurofibromatous type 1 (neurofibromas, gliomasof CNII, lisch nodules and café au lait spots) Neurofibromatous type 2 (acoustic neuromas and multiple meningiomas) Tuberous sclerosis (hamartomas) Von HippelLindau (hemangioblastomas, renal cysts and renal cell carcinoma)

28. Astrocytoma Most common type of glioma Note the secondary brain stem haemorrhage (duret haemorrhage) Look for herniation Red arrow (below) showing infarcted brain parenchyma due to herniation

29. Astrocytoma Note bizarre giant cells, atypical mitoses and proliferated vessels. Below is normal brain tissue for comparison

30. Astrocytoma Another one

31. Colloid cyst of the third ventricle These occur in young adults and may obstruct the foramina of Munro leading to a noncommunicating hydrocephalus and headaches.

32. Meningioma These arise from the arachnoidgranulations and are associated with the dura. Most are parasagittal. They are benign, slow-growing tumours but may invade overlying bone and cause bone thickening. They may present with personality change or focal symptoms caused by compression of the underlying brain. They are usually solitary.

33. Brain Mets Top – small cell lung Ca Below - melanoma

34. Eye tumours Retinoblastoma Mainly a tumour of kids Ocular melanoma

35. Traumatic brain injury Parenchymal injuries include concussion, contusion, laceration and white matter injury. Contusions occur where the brain hits the bones of the skull following a decelerating injury. Contusions at the site of the initial impact represent a coup injury, those on the opposite site, a contre-coup injury. The contrecoup injury is often more extensive. The common sites of injury are the crests of gyriat the tips of the temporal lobes, the inferior frontal surfaces and the occipital poles. Early lesions show oedema and haemorrhage. Old lesions appear as retracted yellow brown patches on the crests of gyri (called plaque jaune) and can be the origin of epileptic discharge. Histologically, the lesions show gliosisand macrophages containing haemosiderin. White matter injury can take the form of diffuse axonal injury deep in the brain. Axonal retraction balls and focal haemorrhages are seen. It is believed mechanical forces damage the integrity of the axons at nodes of Ranvier. These changes are seen in people whose brains are exposed to repeated trauma e.g. ex boxers.

36. Brain injury TOP: Old traumatic brain injury MIDDLE: acute traumatic brain injury. Multiple intracerebral brain haemorrages seen BOTTOM: Old traumatic brain injury

37. Cerebral malaria This man is from PNG. What is the likely organism? Plasmodium falciparum. What do you see? the changes seen are due to plugging of the vessels by infected red cells with secondary hypoxia and small ring haemorrhages. (Note the similar appearance to that seen when fat embolism affects the brain.)

38. Extradural Haematoma Cant cross suture lines Lens shaped, biconcave Also called an epidural haematoma Usually traumatic MOA, rupture of the middle meningeal artery

39. Subdural haematoma Can cross suture lines Rupture of bridging veins, often in elderly Can present weeks/months later Chronic subdural haemorrhage

40. Intracerebral haemorrhage Woman died from a fat embolism after a car accident Note the multiple small haemorrhages and their characteristic location in the white matter, just where it abuts the grey matter.

41. Spinal cord injury Fracture - dislocation of the cervical spine with compression and contusion of the cord.

42. Congenital vascular malformations Absent posterior communicating arteries in the circle of willis Angiomatosis. Haemangiomas were also found elsewhere in the body Vascular malformation

43. Cerebral malaria This man is from PNG. What is the likely organism? Plasmodium falciparum. What do you see? the changes seen are due to plugging of the vessels by infected red cells with secondary hypoxia and small ring haemorrhages. (Note the similar appearance to that seen when fat embolism affects the brain.)