Session 8 - Lecture 3: Neuropathology Flashcards
What is meningitis and what are the main causative organisms?
Inflammation of the leptomeninges (pia and subarachnoid). The meninges become thicker due to inflammation. Neonates = E.coli 2-5 yo = H.influenzae 5-30yo = N.meningitides >30yo = S.pneumoniae Chronic = M.tuberculosis
What are the local complications of meningitis?
Death, infarct, abscess, subdural empyema and epilepsy.
What is encephalitis.
Inflammation of the brain parenchyma, usually caused by a viral agent. Causes neuronal cell death which leads to the formation of inclusion bodies. Lymphocytic inflammatory reaction. Temporal lobe --> herpes virus Spinal cord motor neurones --> polio Brainstem --> rabies CMV --> inclusion bodies
Describe the mechanism behind prion disease.
Prion proteins are a normal constituent of the synapse (PrP). Mutated PrP can be formed sporadically, familial or ingested. Mutated PrP interacts with normal PrP which leads to a post translation conformational change which is a lot more stable. The body does not destroy this mutated PrP as it is not recognised as foreign. The mutated PrP aggregates which leads to neuronal death and leads to holes in grey matter –> spongiform encephalopathy.
Describe the differences between classic and variant CJD.
Classic - median age at death is 68yo, duration is around 4-5 months, variable accumulation of protein.
Variant - median age at death is 28yo, duration is 13-14 months and there is marked accumulation of protein.
Name the different types of dementia.
Alzheimers, vascular, Lewy body, Pick’s disease, frontotemporal and HIV-associated.
Briefly describe the pathophysiology of Alzheimers.
Exaggerated ageing process, reduced brain weight, cortical atrophy with neuronal damage. Formation of neurofibrillary tangles due to hyperphosphorylated Tau proteins which bind to microtubules of neuronal cells –> intracellular twisted filaments. Also the formation of senile plaques which are foci of enlarged axons, synaptic terminals and dendrites within which amyloid is deposited in the centre.
Why can a patient suffering from Down’s syndrome present with early onset Alzheimer’s disease?
Down’s syndrome is a trisomy of chromosome 21. The amyloid precursor protein gene is found on chromosome 21. Presenilin genes 1 and 2 are also located on chromosome 21 which are responsible for production of secretes, an enzyme responsible for the incomplete breakdown of APP leading to amyloid deposition.
What is normal intracranial pressure?
0-10mmHg but can be up to 20mmHg when coughing or straining.
How can the body compensate for a raised intracranial pressure?
By reducing blood volume, reducing CSF volume or spatial brain atrophy.
What is a hernia?
Protrusion of an organ/part of an organ through the wall that normally contains it.
Describe a subfalcine herniation.
Same side as mass, the cingulate gyrus pushes under the free edge of the fall cerebra. This leads to ischaemia of the frontal and parietal lobes, the corpus callosum compresses the anterior cerebral artery leading to an infarct.
Describe a tentorial herniation.
Uncus/medial part of the parahippocampal gyrus pushes through the tentorial notch. This can lead to damage of the occulomotor nerve on the same side and occlusion of blood flow in the posterior cerebral and superior cerebellar arteries. This type of herniation is commonly fatal as can you can get a secondary haemorrhage into the brainstem called a durat haemorrhage which can affect the cardiac and respiratory centres.
Describe a tonsilar herniation.
Cerebellar tonsils push into the foramen magnum compressing the brainstem.
Give an example of a benign and malignant tumour of the brain.
Meningioma - benign and meningeal in origin.
Astrocytoma - malignant and astrocyte origin.
