Key Pathologies Flashcards
Papilloedema
Definition: Bilateral swelling of the optic disc
Aetiology: Raised intracranial pressure (transmitted along the subarachnoid space and causes axoplasmic flow stasis, leading to oedema of the disc)
Signs/symptoms: Cotton wool sports, blurring of disc boundaries, headache, nausea
Risk factors: Conditions/exposure that increases the risk of ICP e.g. head trauma and meningitis
*Avoid lumbar puncture in the presence of papilloedema - indicates raised ICP
Hydrocephalus
Definition: An increased volume of fluid within the ventricular system of the brain
Aetiology:
- Inflammation e.g. meningitis
- Obstruction e.g. space occupying lesion
- Communicative - insufficient resorption of CSF
Signs/symptoms: Headache, vomiting, changes in consciousness, fontanelle enlargement in children, poor feeding, seizures
Pathophysiology: Inabilty of the ventricular system to drain CSF or overproduction of CSF leads to enlargement of the ventricles which in turn displaces/compresses brain tissue
Risk factors:
Investigations:
GBS - Guillain-Barre Syndrome
Definition: An acute inflammatory polyneuropathy of axonal and demyelinating forms. Typically follows gastroenteroitis or influenza-like infection (2/3 of pts have had an infection upto 6 weeks previous to the start of symptoms).
Aetiology: Immune mediated attack on myelin/Schwann cells of sensory and motor neurones - cellular and humoral.
Signs/symptoms: Symmetrical muscle weakness affecting the lower extremities first; motor difficulty; absence of reflexes; paraesthesis without sensory loss (beginning in the hands and feet); flaccid paralysis
Pathophysiology: Autoimmune attack of neuronal schwann cells and axons, may be attributed to molecular mimicry and the production of autoreactive Igs (gangliosides).
Risk factors: Recent infection; trauma; surgical procedures; vaccination
Investigations: Nerve conduction studies; lumbar puncture; LFTs (aminotransferases may be elevated)
Treatment:
If ambulatory within 2 weeks of onset or non-ambulatory within 4 weeks of onset: Plasma exchange
Brown-Sequard spinal lesion
Definition: Rare neurological condition resulting from hemi-section of the spinal cord, leading to hemiparaplegia of one side of the body and sensory loss of the contralateral side of the body.
Aetiology: Spinal cord trauma/lesion (neck or back); spinal cord tumour; ischaemia; infectious/inflammatory disease
Lesion to the right hand side of the neck:
- DCML: Not yet decussated - ipsilateral loss of fine touch etc.
- Spinothalamic tract: Decussated - contralateral loss of pain and temperature
- Corticospinal tract: Already decussated - ipsilateral loss of fine motor control
Signs and symptoms:
Initially: Spinal shock (loss/depression of all sensorimotor function of the spinal cord, below the level of the injury), which may persist for weeks following the injury
Symptoms of LMN at the site of the lesion
Symptoms of UMN lesion below the site of the lesion
Ipsilateral Horner’s syndrome - if lesion/trauma occurs above T1
Risk factors:
Investigations: Sensation, motor and reflex testing
Treatment:
- Rehabilitation
- Treatment of spasticity: Baclofen (GABA agonist - general) or botulinum toxin (pre-synaptic membrane to prevent NT release - local)
Eye pathology
Pupillary constriction/dilation; CNs VI, IV and III
Pupil constriction → Medical cause
Pupil dilation → Surgical cause
CN III (oculomotor nerve):
Paralysis of the levator palpebrae muscle leads to ptosis (drooping of the eyelid)
Paralysis of sphincter pupillae leads to dilation of the pupil
Paralysis of MR, SR, IR and IO leaves the actions of the SO unopposed hence, the eye adopts a ‘down and out’ appearance - type of divergent squint
CN IV (trochlear):
Paralysis of the superior oblique muscle causes the eye to adopt a hypertropic position (more elevated than normal).
Loss of intorsion from SO causes the pt to tilt their head away from the side of the lesion
CN VI (abducens):
Paralysis of lateral rectus leads to an inability to abduct the eye.
Horizontal diplopia may be experienced, with the sensation worsened by looking towards the side of the lesion
Bulbar and pseudobulbar palsy
Bulbar palsy: LMN palsy of the CNs IX, X and XII
- Nasal voice
- Flaccid paralysis, fasciculations and atrophy of the tongue
- Reduced gag reflex
Pseudobulbar palsy: UMN palsy of CNs V, VII, IX, X and XII
- Monotone high-pitched voice (Donald Duck)
- Initially presents as LMN with progression to UMN - medical emergency as can lead to dysphagia
- Increased gag and jaw jerk reflexes
- UMN paralysis of the face
Meningitis
Definition: Inflammation of the meningeal covering of the CNS
Aetiology: Bacterial (meningococcal/pneumococcal/HiB) or viral infection
Signs and symptoms:
Triad = Headache, photophobia and neck stiffness
- Headache
- Photophobia
- Signs of meningeal irritation: Neck stiffness, positive Kurnig’s and Brudzinski’s signs
- Signs of raised ICP: Vomiting, papilloedema
- Ruchal rigidity
- Fever
- Seizures
Pathophysiology: Infection of the subarachnoid space leads to inflammation of the meninges. Inflammatory exudate accumulates causing meningeal irritation and increased ICP. Arterial supply to the cerebrum may be compromised, through compression.
Risk factors:
- Extremes of age (< 5 or < 65)
- Shared accomodation
- Exposure to others with the condition
- Immunodeficiency
Investigations:
Lumbar puncture is contraindicated in the presence of raised ICP:
CSF pressure is increased in bacterial meningitis.
Glucose and glucose CSF:serum ratio are both decreased in bacterial meningitis.
Glucose CSF:serum ratio is increased in viral meningitis.
WCC is increased in both bacterial and viral.
CT/MRI scan
Treatment:
- Dual antibiotic therapy - Vancomycin and ceftriaxone
- Steroids (dexamethasone) - Reduces neurological deficits
Epidemiology:
Incidence greatest amongst young children.
Decreased incidence due to the introduction of vaccination (HiB)
Epilepsy Classification
Focal, generalised and unknown onset
Multiple Sclerosis
x
Parkinson’s disease
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Trigeminal neuralgia
Definition: Facial pain syndrome in the distribution of 1 or more branches of the trigeminal nerve. Characterised by sharp, intense stabbing pain for < 2 minutes or constant facial pain in the absence of neurological deficit.
Aetiology:
Trigeminal nerve compression - majority of patients
Compression of the trigeminal nerve at its point of exit by an aberrant vascular loop, typically the superior cerebellar artery.
Demyelinating disease e.g. MS
Signs/symptoms:
- Unilateral pain lasting seconds to minutes - described as sharp/stabbing/burning
- Triggers such as tooth brushing, eating and cold
- Completely unremarkable physical and neurological examination
Pathophysiology:
Focal demyelination and the resultant conduction abnormalities are thought to represent the mechanism of neuropathic pain in trigeminal neuralgia - seen at the root entry zone.
Plaques have been identified in association with MS
Risk factors: Increased age; MS
Investigations:
- Examine TMJ, temporal arteries, dentition
- Usually clinical diagnosis.
- Intra-oral X-ray & MRI may be considered
Treatment:
Anticonvulsants - Carbamazepine
Microvascular decompression for ongoing TN
Epidemiology:
Rates increase with age. Slight female predominance.
Stroke
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Ataxia
Definition: A neurological syndrome characterised by incoordination or clumsy movement of the limbs, trunk and cranial nerves. The syndrome results from defects in the cerebellum and its connections or in the proprioceptive sensory pathways (sensory axtaxia?).
Sensory ataxia is characterised by incoordination of the upper and lower limbs associated with a lack of proprioception.
Aetiology: May be acquired or genetic.
Acquired causes: Vascular, demyelinating, autoimmune, compressive etc.
Signs/symptoms:
DANISH - cerebellar dysfunction
(dysdiadochokinesia, ataxia, nystagmus, intention tremor, scanning speech. hypotonia)
Risk factors:
Investigations: Imaging (check for cerebellar atrophy); reflexes
Treatment:
Epidemiology:
