Neurology and microbiology and haematology Flashcards
Label the constituent portions of the cerebral cortex
Frontal - Contains motor cortex (anterior to central sulcus). Also has large influence on all executive control. Contains Brocas area for speech.
Parietal - Contains main somatosensory area. Also involved in calculation and the non-dominant lobe is responsible for spatial awareness and positioning.
Occipital - Mainly involved in vision
Temporal - Contains Werneckes area superiorly. Involved in emotion, memory, olfaction and auditory capabilities.
Describe the syndromes that would arise from a lesion in cerebral hemispheres
Focal neurological deficits:
Damage to the Premotor cortex would result in apraxia (inability to execute movements)
Damage to Temporal lobe could result in amnesia.
Damage to the language area may give aphasia or dysphasia.
Damage to parietotemporal cortex will give agnosia (inability to recognise).
Describe the syndromes that would arise from a lesion in brainstem
Depends on where the lesion is:
May result in Problems with sleep/wake cycle, balance, cardioresp control os reticular formation affected.
If cerebellar communicants affected then cerebellar symptoms will persist.
Cranial nerves may also be affected
Describe the syndromes that would arise from a lesion in the cerebellum
Dysdiadochokineses Ataxia Nystagmus Intention tremor Slurred speech (dysarthria) Hypotonia
IPSILATERAL
Describe the syndromes that would arise from a lesion in the basal ganglia
Parkinsons - Tremor Rigidity Akinesia Postural instability
Huntingtons:
Dyskinesia
Chorea
Athetosis (serpentine twisting)
Tourette’s:
Tics
Name the location of the causative lesion in homonymous hemianopia
Lesion from optic radiation to the visual cortex
Name the location of the causative lesion in bitemporal hemianopia
Optic chiasm
Describe the clinical difference between upper and lower motor neuron facial weakness
The forehead is spared in an unilateral UMN lesion to CNVII.
Describe the clinical difference between upper and lower motor neuron limb weakness, with specific reference to findings on inspection, tone, deep tendon reflexes and pattern of weakness.
UMN: Decreased power, (weakness in extensors - upper limbs and flexors - lower limbs = pyramidal weakness. strength in antigravity muscles) increased tone, increased reflexes No wasting Spaticity (clasp knife) Extensor plantar response Loss of abdominal reflexes
LMN Decreased power Decreased tone Decreased reflexes Wasting plegia and paresis of specific muscles.
Describe the clinical syndrome that would arise from C5 lesion
Sensory loss to lateral part of arm
Loss of biceps reflex
Motor loss: Shoulder abduction and elbow flexion
Describe the clinical syndrome that would arise from median nerve lesion
Sensory loss to palmar side of first 3.5 digits - paraesthesia
Motor loss: Wasting of pollicis brevis.
Patient wakes up at night with pain/paraesthesia radiating down forearm into hand. Relieved by hanging arm down.
RFs: RA, pregnancy, hypo T4, obesity, acro, dialysis
Describe the clinical syndrome that would arise from an ulnar nerve lesion
Sensory loss to median 1.5 digits
Wasting of hypothenar muscles, interossei, medial 2 lumbricals.
Describe the clinical syndrome that would arise from a radial nerve lesion
Sensory loss to the dorsum of the hand
Motor loss to brachoradialis and finger extensors
Compression of nerve against humerus leads to wrist drop.
Describe the clinical syndrome that would arise from a S1 nerve root lesion.
Sensory loss to posterior of calf and lateral border of foot.
Loss of ankle reflex.
Loss of plantar flexion.
Sudden onset during lifting/bending/twisting.
Define cerebrovascular disease with specific reference to time course
Stroke - Loss of cerebral function lasting >24 hours or leading to death, with no other cause than a vascular one.
TIA - A focal neurological deficit lasting seconds to 24hrs, with complete recovery.
Amaurosis fugax - Temporal loss of vision in one eye prior to a carotid system TIA.
List the irreversible 8 and reversible 10 risk factors leading toward the development of stroke
Reversible: Cholesterol, obesity, T2DM, hypertension, smoking, carotid stenosis, sleep apnoea, endocarditis, neurosyphilis, COX-2 inhibitors.
Irreversible: Age, gender, SLE, AF, thrombohilia/hyperviscosity, amyloidosis, hyperhomocysteinaemia, migraine
Describe the pathological causes and consequences of ischaemic stroke
Caused by local arterial disease. Rupture of atheromatous plaque, eventually causing ischaemia of the effected area. Emboli from the heart common -
AF. Unlikely to be cause by stenosis - Although a slight drop in BP can result in watershed effect.
Initially little evidence of infarction. 24 hrs after onset, boundary between white and grey matter become blurred. Eventually necrotic material begins to organise and macrophages infiltrate and oedema lessens. Eventually ischaemic area shrinks and ventricle enlarges to fill area.
Describe the pathological causes and consequences of haemorrhagic stroke.
Most commonly occurs in hypertensive patients.
Microaneursyms develop and when they rupture blood is released which eventually may form a haemotoma (often in MCA branches to BG, pons and cerebellum) if death does not ensue.
Headach - increased ICP - death. Result is a cyst, containing yellow-brown fluid, walled by glia.
Describe how atrial fibrillation gives rise to stroke
Blood is turbulent and relatively static in the atria giving rise to thrombus formation. 80% of strokes are due to thromboemboli and 70% of TIAs.
Describe the clinical presentation of a subarachnoid haemorrhage, with specific reference to features in the history and examination including the rate of onset of symptoms, and signs arising from the event.
Sudden onset of a thunderclap headache, followed by nausea and vomiting. Coma and death may then follow. Other signs and symptoms: Neck stiffness Positive Kernigs sign Pappiloedema Photosensitivity Brudzinskis signs: flexion of the elbow in response to pressure to the cheek; flexion of the hip in response to flexion of the neck, and abduction and flexion of the hip in response to pubic symphysis pressure.
Describe the clinical features of meningism
Neck stiffness
Headache
Photophobia
Describe the vascular abnormalities which may predispose a patient to developing a subarachnoid haemorrhage.
Berry aneurysm - Congenital weakness in the elastic tissue surrounding arteries
Most common at branch points
May be multiple in number
Arteriovenous malformations - Abnormality in the arterio-venous connections causing rupture due to the abnormal pressure distribution.
List the potential complication of a subarachnoid haemorrhage.
Increased ICP Arterial spasm Subdural haemorrhage Coma Death
List the predisposing factors which make a patient vulnerable to developing subdural haemorrhage
Elderly
Alcoholic
Anticoagulant therapy
Describe the clinical presentation of a chronic subdural haemorrhage
May present with a long prodome Time between initial trivial trauma and SBH may be weeks. Headache, drowsiness, confusion, coma stupor Focal deficits
