Neurology Flashcards
What is a Functional Neurological Disorder?
“the interface between neurology and psychiatry”
This is a disorder in the signalling between the body and the brain resulting in miscommunication and misinterpretation of signals. The brain becomes “stuck” in abnormal patterns resulting in a very real selection of symptoms:
- Motor dysfunction: dystonia, weakness, paralysis, jerky movements (myoclonus), gait disorder and speech/swallowing difficulties e.g. slurring and choking
- Sensory dysfunction: numbness/tingling often unilateral, loss of vision or double vision
- Episodes of altered awareness: dissociative (non-epileptic) seizures, blackouts and faints.
These can combine in many ways and symptoms may be triggered by preceding illness such as physical injury, infection, panic attack and migraine. Chronic pain, headache, migraines and fatigue may also be presenting features.
No structural issues detected on MRI or EEG (all normal) although issues may be detected if patient has pre-existing neurological condition.
FND is as common as MS and Parkinson’s disease (accounts for 1/6th of outpatient visits).
Physio and CBT are the main treatment options to attempt to ‘re-wire’ the brain
How is a dissociative seizure recognised?
A seizure with violent limb thrashing that lasts for >5 mins and eyes remain closed throughout, side-to-side head movements, hyperventilation during or tearful on recovery. Attacks can be even longer, lasting 10-20 mins
What is GABA?
The main inhibitory neurotransmitter in the brain. Glutamate is the excitatory neurotransmitter. GABA will increase potassium efflux and decrease calcium entry to the neuron and prevent release of excitatory neurotransmitters.
This process is harnessed in the treatment of epilepsy in the aim of increasing the concentration of GABA (inhibitory neurotransmitter) in the neuron and preventing excess excitation.
What are the different types of epileptic seizure?
Focal (partial): simple = no LOC ; complicated = LOC
Generalised: atonic, absence, myoclonic, tonic and tonic-clonic
Focal can evolve into generalised and is normally caused by structural disease e.g. hippocampal sclerosis is a common cause of temporal lobe epilepsy that is resistant to treatment will present with verbal or visual memory deficit.
Focal onset epilepsy?
Underlying structural cause with symptoms of the area affected.
Can generalise (secondary generalised)
Onset at any age
Treat with Carbamazepine or lamotrigine
Commonly seen: complex partial seizure with hippocampal sclerosis
What can precede hippocampal sclerosis?
Febrile seizures in youth - sustained more harmful
Primary generalised epilepsy?
Often present as child/teen.
Example: juvenile myoclonic epilepsy with early morning jerks, generalised seizures, RF=sleep deprivation, flashing lights, alcohol
Sodium valproate is the main treatment option in PGE - although lots of SE and teratogenic.
Absence = ethosuximide or SV (AVOID carbamazepine as can induce status epilepticus)
Myoclonic = Levetiracetam or SV (AVOID carbamezapine as this can induce a GTC), lamotrigine can also be used
GTC and Atonic = lamotrigine or SV
What are some considerations for women on anti-epileptic medications?
Many are enzyme inducers so will prevent hormone contraception and morning after pill from working. (cabamezapine, phenobarbital, phenytoin, topiramate)
SV is teratogenic as inhibits folic acid synthesis.
Require pre-conceptual counselling.
What is status epilepticus?
Continued seizure state for >30 mins despite interventions or recurrent seizures without recovery between.
- Generalised convulsive status epileptica
- Non-convulsive status = “altered state but not convulsing”
- Epilesia partials continua = consciousness maintained but continued partial seizure activity.
Precipitants: head injury, infection, SAhaemorrhage, severe metabolic disorder, withdrawal of AED, treatment of absence or myoclonic with carbamazepine.
Excess cerebral energy demand and poor substrate delivery results in lasting damage with hypoxia, hypotension, hyperthermia and rhabdomyolysis.
What is a glioblastoma multiform, presentation, diagnosis and treatment?
Brain tumour with the worst prognosis, commonly death within 15 months from detection. It is also referred to as a Grade IV astrocytoma and is a tumour involving the glial cells (astrocytes and oligodendrocytes). This can be primary or evolve from lover grade astrocytomas. A key feature is the ability to extend tumour cells into the surrounding brain tissue.
Often found in the frontal, temporal or occipital lobes in patients aged 45-70. Presentation: - persistent headaches - new onset seizures - vomiting - lack of appetite - change to mood/personality - gradual change to speech and language - changes to vision (double or blurred) - change in congnition e.g. carry out and learning new skills
Diagnosis: based on history, examination and CT/MRI scan for tumour localisation. Magnetic resonance spectroscopy for chemical composition of tumour. Tumour biopsy to stage and type. PET for tumour recurrence.
Treatment:
- Surgery (debulking)- this is the mainstay of treatment as the tumour mass can impact brain function through direct pressure or oedema increasing ICP. This removes the bulk of the tumour and can make the tumour more responsive to treatment (as you remove the resistant cells in the centre). Debulking reduces ICP and increases survival/QOL but is not curative. GBM are notorious for infiltrating surrounding tissue so impossible to get clear margins (microscopic tumour invasion)
- External beam radiotherapy - 10-30 doses
- Chemotherapy with temozolomide
- Other treatments are for recurrent or resistant tumours and are based around clinical trial e.g. gene therapy, intra-operative radiotherapy, immunotherapy
Challenges with treatment:
- Localisation of the tumour
- Inherent tumour resistance
- Odema caused by capillary leakage, increases ICP
- Blood supply in the tumour is variable, resulting in inefficient delivery of chemotherapeutic medications
- Migration of tumour cells into surrounding brain tissue
- neurotoxicity from drugs
What is discectomy/laminectomy?
Discectomy - the removal or partial removal of a intervertebral disc due to compression on the spinal cord. Depending on the location of the compression pain and numbness/weakness will be felt in certain areas e.g. S1 will have posterior leg pain originating in the buttocks and extending all the way to the plantar surface of the foot.
Laminectomy - is the removal of a lamina from the vertebrae to release pressure on the spinal cord or to gain access to the spinal cord.
What are risk factors for back pain?
Mechanical injury from sports/work, twisting and lifting heavy items, obesity, osteoporosis and early osteoarthritis, periods of physical inactivity, spondylosis
What is spondylosis?
The loss of water content in the intervertebral discs resulting in loss of cushioning effect. This causes secondary OA. It is usually normal as part of the ageing process.
If in the cervical spine it will cause neck stiffness and pain that radiates to the shoulder and occiput
What is ‘Mechanical Back Pain’?
Pain caused by physical activity, obesity etc that is made worse on movement and better with rest. No red flags are present (caudal equine, weight loss, chest pain, fever, malaise, lump/deformity, difficulty sleeping due to pain, worse on coughing/sneezing/poop).
Treatment is with analgesia and physiotherapy only. Some may be suitable for surgery if the degeneration is localised e.g. to L4/5, but outcomes of surgery are minimal 5 years later.
Bed rest is not recommended as this increases stiffness and
Acute disc tear
Occurs when the outer annulus fibrosis tears (this is rich with nerves). It usually occurs after lifting heavy objects and pain is worse on coughing.
Pain will subside but may take around 2-3 months to fully recover
Treatment is with physiotherapy and analgesia
