Neuro Flashcards
(309 cards)
1
Q
Red flags for headaches:
A
- Thunderclap
- Refractory pain
- Progressive or persistent daily headache
- Papilloedema
- Features of raised ICP
- Visual loss
- Scalp tenderness
- Atypical aura or duration
- Progressive neurological deficit
- Unexplained cognitive or behavioural change
- Cancer history or immunosuppression
2
Q
Acute change in cognition and behaviour with headache:
A
Encephalitis
3
Q
Scalp tenderness with headache think…
A
GCA / Temporal arteritis.
4
Q
Indications that a patient is suffering from a medication overuse headache.
A
- Headache occurs 15 days or more per month and
- Has been using regular acute / symptomatic headache medication for 3
- months (“regular” = 10+ days per month of ergotamines, triptans, opoids OR
- 15+ days per month of simple paracetamol or NSAIDs) and
- No other headache diagnosis more appropriate
5
Q
What class of medication is topiramate?
- When is it used?
- Contraindications?
A
Anti-epileptic
- Used for migraine
- Contraindicated in pregnancy
Note: Also causes weight gain.
6
Q
What are Monoamine oxidase inhibitors and COMT inhibitor used for what and how do they work?
A
Used to treat parkinson’s by preventing the breakdown of dopamine.
7
Q
Common side effects of Ldopa:
A
- Hypotension
- Restlessness
- Gastrointestinal upset
- In rare cases, dopamine excess can result in psychiatric reactions including acute psychosis.
8
Q
Summarise the classic presentation of a cluster headache:
A
This is the classic presentation of cluster headaches. They tend to present as unilateral peri-orbital headaches and are associated with ipsilateral ptosis, lacrimation, conjunctival injection and rhinorrhea. They classically occur in clusters over a few weeks, with a “silent” period in between them in which the patient does not experience headaches
9
Q
A 65-year-old lady presents to her GP with a new-onset left-sided lower motor neuron facial palsy and mild-to-moderate left-sided otalgia. She suffers from hypertension and diverticular disease. On examination there is a tender vesicular rash found inside the external auditory canal on the left-side; the right side is normal. Hearing appears normal for her age.
What is the most likely diagnosis?
A
Ramsay Hunt Syndrome type II
This is the correct answer. Ramsay Hunt syndrome type II is a reactivation of varicella zoster virus in the geniculate ganglion. It causes a unilateral acute facial nerve paralysis in addition to an erythematous vesicular rash in the ear canal. Occasionally otalgia precedes the rash and facial palsy.
10
Q
Negative findings on CT for someone with a thunderclap headache… what’s next?
- what are you looking for?
A
LP looking for presence of RBC’s and xanthocromia.
11
Q
What is xanthochromia?
A
Xanthochromia is the presence of bilirubin in the cerebrospinal fluid and is sometimes the only sign of an acute subarachnoid hemorrhage
12
Q
Extradural haematoma is classically due to injury to what artery?
A
Classically due to injury of the middle meningeal artery, a branch of the maxillary artery (from the ECA).
13
Q
EDH vs SDH findings on CT
A
EDH = lemon shaped does not cross sutures.
SDH = Cresecent shaped, does cross sutures.
14
Q
What is the most common primary brain tumour?
A
Glioblastoma multiforme
15
Q
Summarise meningiomas:
A
Meningiomas are typically benign, extrinsic tumours of the central nervous system. They arise from the arachnoid cap cells of the meninges and are typically located next to the dura and cause symptoms by compression rather than invasion.
16
Q
What is the most common primary brain tumour in children.
A
Pilocytic astrocytoma
17
Q
Treatment for pituitary adenoma:
A
Treatment can either be hormonal or surgical (e.g. transphenoidal resection).
18
Q
What hereditary syndromes cause brain tumours?
A
Neurofibromatosis
Tuberous sclerosis
19
Q
How glioblastoma’s appear on CT/MRI imaging?
A
On imaging they are solid tumours with central necrosis and a rim that enhances with contrast. Disruption of the blood-brain barrier and therefore are associated with vasogenic oedema.
20
Q
Where are meningiomas typically located?
A
They typically are located at the falx cerebri, superior sagittal sinus, convexity or skull base.
Often stuck on the outside.
21
Q
Tumours that commonly metastasise to the brain:
A
lung (most common)
breast
bowel
skin (namely melanoma)
kidney
22
Q
1p 19q deletion = what cancer?
A
Oligodendroglioma
23
Q
1DH1 mutation = what brain tumour?
A
Astrocytoma
24
Q
MGMT promoter methylation is seen in what brain tumour?
A
Glioblastoma
25
What is the issue with benign brain tumours?
* Grow by expansion, compressing surrounding structures.
* Some invade surrounding brain / blood vessels / tissues
* Can be difficult to get to, and / or remove.
26
Most common primary source of secondary brain mets?
Lung cancer (SCC)
27
Most common location in the brain for brain mets?
Cerebrum 80%
Cerebellum 15%
Brain stem 5%
28
What are the two main drugs used in the management of brain cancer?
Dexamethasone
Anti-epileptics
29
Best imaging for brain tumours?
MRI!
- Shows the anatomy better.
- Functional MRI looking at primary cortical areas.
30
Rule of thirds for brain mets:
1/3 = 1 met
1/3 = <4 mets
1/3 >4mets :(
31
How to decide who to treat with brain mets?
Only aim to treat patients with less than 4 brain mets.
Need to assess performance score.
32
When to biopsy for brain cancer?
When surgery / resection isn't possible.
33
When are awake surgeries helpful?
When the tumours are located in the speech areas of the brain.
34
Chemotherapy drugs used for brain cancers:
Temozolamide
PCV (Procarbazine, CCNU, Vincristine)
Lomustine alone
Other
* Avastin - controls oedema around the tumour.
* Tamoxafen
35
Mainstay of treating brain cancers:
Radiotherapy!
Note: Radiosurgery is sometimes used for patients to give a focused dose to small lesions (mets/meningiomas).
36
Clinical features of encephalitis:
ALTERED MENTAL STATUS
Other suggestive features include fever, a flu-like prodromal illness, and early seizures.
37
What is the most common cause of encephalitis?
HSV-1
- responsible for 95% of cases in adults.
This said HSV-2, cytomegalovirus, epstein barr virus, varicella-zoster virus, HIV and the arboviruses (including west nile virus) can also cause a similar picture.
38
Where in the brain is typically affected in encephalitis?
Temporal and inferior frontal lobes
39
What investigations should be carried out for encephalitis?
LP - CSF shows:
Lymphocytosis
Elevated protein
PCR for HSV, VZV and enteroviruses.
Neuroimaging - MRI
Medial temporal and inferior frontal changes (e.g. petechial haemorrhages)
normal in one-third of patients.
40
Treatment for encephalitis:
Aciclovir
Ceftriaxone
41
Treatment of encephalitis including doses:
2g IV ceftriaxone BD
10 mg/kg aciclovir TDS for two weeks.
42
What is meant by encephalopathy?
Clinical syndrome of altered mental status; manifesting as reduced consciousness or altered cognition, personality or behaviour.
Has many causes including systemic infection, metabolic derangement, inherited metabolic
encephalopathies, toxins, hypoxia, trauma, vasculitis, or central nervous system infection.
43
What is meant by encephalitis??
Inflammation of the brain
Strictly a pathological diagnosis; but surrogate clinical markers often used, including CSF
inflammatory change or changes on neuroimaging
Causes include viruses, small intracellular bacteria that directly infect the brain
parenchyma and some parasites
Can also occur without direct brain infection, for example in acute disseminated
encephalitis myelitis (ADEM), or antibody-associated encephalitis.
44
What is Cushing's triad?
Bradycardia, irregular respiration, wide pulse pressure.
The triad represents raised ICP.
45
When to delay lumbar puncture in encephalitis?
Get imaging first in GCS less than 14.
Bleeding disorders.
Immunocompromised.
Signs of raised ICP - papilloedema, cushing's triad.
Focal neurological signs, recent onset seizures.
46
CSF findings in encephalitis:
CSF is gin clear
Slightly increased cells 5-1000, predominantly leucocytes
Normal CSF / Plasma glucose ratio
47
CSF findings in bacterial meningitis:
CSF cloudy.
High cell count (neutrophils).
High protein.
48
What is seen on an MRI for MS patients?
Typically periventricular white matter lesions are seen on MRI.
49
Acute managment of MS:
Methylprednisolone
Must rule out infection first
50
How are the treatment for chronic MS divided?
Disease modifying drugs
Symptomatic therapies
51
What disease modifying drugs are used to manage MS?
- First-line injectables such as beta-interferon and glatiramer
- New oral agents such as dimethyl fumarate, teriflunomide and fingolimod
- Biologics such as natalizumab and alemtuzumab.
52
Symptomatic therapies for chronic MS:
- Physiotherapy
- Baclofen and BoTox for spasticity
- Modafinil and exercise therapy for fatigue
- Anticholinergics for bladder dysfunction
- SSRIs for depression
- Sildenafil for erectile dysfunction
- Clonazepam for tremor
53
Clinical features of essential tremor:
- postural tremor: worse if arms outstretched
- improved by alcohol and rest
- most common cause of titubation (head tremor)
54
Management of essential tremor:
Propanolol
Behavioural techniques and physical therapy
55
Parkinson's triad:
Asymmetric tremor, rigidity and bradykinesia
56
Features of a cerebellar tremor:
including examination
Intention tremor
Cerebellar signs e.g. Past-pointing, nystagmus etc
57
Mnemonic to remember features of cerebellar dysfunction:
DANISH
- Dysdiadochokinesia (an inability to perform rapid alternating hand movements)
- Ataxia (a broad-based, unsteady gait)
- Nystagmus (involuntary eye movements)
- Intention tremor (seen when the patient is asked to perform the 'finger-nose test')
- Slurred speech
- Hypotonia
58
Causes of cerebellar dysfunction:
Vitamin C
The differentials of cerebellar dysfunction can be remembered by going through a surgical sieve (remembered by the mnemonic: VITAMIN C):
- Vascular causes include stroke (ischaemic or haemorrhagic affecting the posterior circulation).
- Infective causes include Lyme disease.
- Inflammatory causes include multiple sclerosis.
- Traumatic causes include trauma to the posterior fossa.
- Metabolic causes include alcoholism.
- Iatrogenic causes include drugs such as phenytoin and carbamazepine.
- Neoplastic causes include primary tumours (e.g. cerebellopontine angle tumour, acoustic neuroma) and secondary tumours (metastases e.g. breast cancer, lung cancer).
- Congenital/hereditary causes include Friedrich's ataxia, and the spinocerebellar ataxias.
59
Most common cause of cerebellar dysfunction:
Stroke
MS
60
What are the different causes tremor?
Essential tremor
Cerebellar dysfunction (intention tremor
Idiopathic (PD) (resting rolling pill tremor)
61
Explain the clinical features of Brown-Sequard syndrome:
Disruption of descending lateral corticospinal tracts, ascending dorsal column and ascending spinothalamic tracts leads to the following findings below the level of the injury:
- Ipsilateral hemiplegia
- Ipsilateral loss of proprioception and vibration
- Contralateral loss of pain and temperature sensation
62
Common causes of Brown-Sequard syndrome:
Common causes of BSS include:
- Cord trauma (penetrating injuries being the most common)
- Neoplasms
- Disk herniation
- Demyelination
- Infective/ inflammatory lesions
- Epidural hematomas
63
Explain the management of Brown-Sequard syndrome:
Management of BSS depends on the causative pathology. Need for conservative or surgical management depends on patient's neurological status and clinico-radiological findings. Surgery intervention is advised in post-traumatic BSS if there is presence of retained foreign objects, CSF leakage, infection or signs of extrinsic spinal cord compression.
Medical management is preferred for infective/ inflammatory or demyelinating causes of BSS while surgical treatment is performed for pathologies causing extrinsic cord compression.
64
Important investigations for epilepsy:
An electroencephalogram (EEG) can show typical patterns in different forms of epilepsy and support the diagnosis.
An MRI brain can be used to visualise the structure of the brain. It is used to diagnose structural problems that may be associated with seizures and other pathology such as tumours.
Other investigations can be used to exclude other pathology, particularly an ECG to exclude problems in the heart.
65
What is meant by 'tonic clonic'
Tonic = muscle tensing
Clonic = muscle jerking
66
First and second line management of tonic clonic seizures:
- First line: sodium valproate + Levetiracetam
- Second line: lamotrigine or carbamazepine
67
Where do focal seizures start and what do they effect?
Focal seizures start in the temporal lobes. They affect hearing, speech, memory and emotions.
68
How can focal seizures present?
- Hallucinations
- Memory flashbacks
- Déjà vu
- Doing strange things on autopilot
69
Treatment of focal seizures:
One way to remember the treatment is that they are the reverse of tonic-clonic seizures:
- First line: carbamazepine or lamotrigine
- Second line: sodium valproate or levetiracetam
70
Summarise absence seizures:
Absence seizures typically happen in children. The patient becomes blank, stares into space and then abruptly returns to normal. During the episode, they are unaware of their surroundings and won’t respond. These typically only lasts 10-20 seconds. Most patients (> 90%) stop having absence seizures as they get older.
Management is: sodium valproate or ethosuximide
71
Summarise atonic seizures:
Atonic seizures are also known as “drop attacks”. They are characterised by brief lapses in muscle tone. These don’t usually last more than 3 minutes. They typically begin in childhood. They may be indicative of Lennox-Gastaut syndrome.
Management is:
- First line: sodium valproate
- Second line: lamotrigine
72
Summarise myoclonic
Myoclonic seizures present as sudden brief muscle contractions, like a sudden “jump”. The patient usually remains awake during the episode. They occur in various forms of epilepsy but typically happen in children as part of juvenile myoclonic epilepsy.
73
What is 'West syndrome'?
West syndrome aka infantile spasms is a rare (1 in 4000) disorder starting in infancy at around 6 months of age. It is characterised by clusters of full-body spasms. There is a poor prognosis: 1/3 die by age 25, however, 1/3 are seizure-free. It can be difficult to treat but first-line treatments are:
- *Prednisolone*
- *Vigabatrin*
74
Complications of sodium valproate:
- Teratogenic so patients need careful advice about contraception
- Liver damage and hepatitis
- Hair loss
- Tremor
There are a lot of warnings about the teratogenic effects of sodium valproate and NICE updated its guidelines in 2018 to reflect this. It must be avoided in girls or women unless there are no suitable alternatives and strict criteria are met to ensure they do not get pregnant.
75
Describe the muscle weakness seen in Bell's Palsy:
Acute (but not sudden) onset, unilateral, lower motor neuron facial weakness, sparing the extraocular muscles and muscles of mastication.
76
What features are suggestive of Ramsay hunt syndrome in place of Bell's palsy?
Features particularly suggestive of Ramsay-Hunt Syndrome include: prominent otalgia, and vesicular rash in the external auditory meatus, palate or tongue.
77
Damage to what nerve presents with foot drop?
Common fibular nerve (common peroneal nerve)
The common peroneal nerve winds round the head of the fibula and is commonly damaged with fractures of the fibular head. It supplies the tibialis anterior muscle (via it's branch the deep peroneal nerve). This muscle dorsiflexes the ankle and therefore damage to its innervation leads to foot drop.
UFC!
78
Explain how status epilepticus is defined but also approached!
Status epilepticus is defined as a seizure lasting >5 minutes, or multiple seizures over 5 minutes with incomplete resolution.
Guidelines have changed
79
How is early status epilepticus treated?
- If in the community:
- Buccal Midazolam or Rectal Diazepam
- If IV access is obtained and resuscitation facilities are available:
- Lorazepam (intravenous) 0.1 mg/kg (usually a 4 mg bolus, repeated once after 10−20 minutes; rate not critical).
80
How is established status epilepticus (0-60mins) treated if not responding to 2 doses of benzodiazepine, give any of the following as second-line treatment
- Levitiracetam
- Phenytoin
- Sodium Valproate
81
How is refractory status treated? (30-90mins)
- General anaesthesia, with one of:
- Propofol (1–2 mg/kg bolus, then 2–10 mg/kg/hour) titrated to effect
- Midazolam (0.1–0.2 mg/kg bolus, then 0.05–0.5 mg/kg/hour) titrated to effect
- Thiopental sodium (3–5 mg/kg bolus, then 3–5 mg/kg/hour) titrated to effect; after 2–3 days infusion rate needs reduction as fat stores are saturated
- Anaesthetic continued for 12−24 hours after the last clinical or electrographic seizure, then dose tapered.
82
What are the most important initial investigations to do in someone presenting with status?
Blood sugar and O2 sats
The most important initial investigations are to check the patient's oxygen saturations and blood sugar level, as these are a common and rapidly reversible cause of seizure activity.
83
Additional management for status in an alcoholic?
IV pabrinex prior to the administration of glucose to avoid precipitation of Wernicke's encephalopathy or Korsakoff's syndrome.
84
Note additional investigations that should be carried out in status:
First line blood tests should include an arterial blood gas, and a routine panel of venous bloods including FBC, U&E, LFT, CRP, Calcium and magnesium, and clotting. Patients should have a serum and urine save for toxicology, and antiepileptic drug levels should be sent as appropriate.
85
Treatment for GBS?
Immunoglobulin and Plasmapheresis are the treatment options, ideally before the ascending weakness causes paralysis of respiration. The sensory disturbance described is dysaesthesia which is also seen in GBS.
86
What is GBS and what is it caused by?
GBS is an ascending inflammatory demyelinating polyneuropathy.
Typically 1-3 weeks after infection (e.g. Campylobacter, mycoplasma, EBV). 40% of cases are idiopathic.
87
How does GBS present?
Progressive ascending symmetrical limb weakness (affecting the lower limbs first). Paraesthesia may precede the onset of motor symptoms. Respiratory muscles may be affected in severe cases. Some cases present with symptoms of cranial nerve palsies (e.g. diplopia, facial droop).
Lower motor neurone signs in the lower limbs (hypotonia, flaccid paralysis, areflexia). Cranial nerve signs may also be present (e.g. ophthalmoplegia, lower motor neurone facial nerve palsy, bulbar palsy) as well as signs of type 2 respiratory failure due to respiratory muscle weakness (e.g. CO2 flap, bounding pulse). Autonomic dysfunction may be present (e.g. arrhythmia, labile blood pressure).
88
Investigations carried out for GBS:
Bedside tests include spirometry (checking for a reduced FVC). Bloods include an ABG (to check for type 2 respiratory failure) and anti-ganglioside antibodies. Other investigations include a lumbar puncture which typically shows a raised protein, with normal cell counts and glucose (so called albuminocytological dissociation).
89
What is Miller-Fisher syndrome?
Miller-Fisher syndrome is a variant of GBS that presents with ataxia, ophthalmoplegia, and areflexia.
The condition is typically positive for anti-GQ1b antibodies.
90
Malingering
Malingering is the deliberate faking of symptoms in order to obtain secondary gain.
91
What is the most common form of occupational focal dystonia?
Writer's cramp is the most common form of occupational focal dystonia. It typically only occurs with a specific action. Dystonia is a sustained muscle contraction often with slow, twisting or repetitive movements or abnormal postures
92
Management for myasthenia gravis:
Management is with prednisolone (acutely) and cholinesterase inhibitors e.g. pyridostigmine or neostigmine (long-term)
92
Management for myasthenia gravis:
Management is with prednisolone (acutely) and cholinesterase inhibitors e.g. pyridostigmine or neostigmine (long-term)
93
How to distinguish an L5 root lesion from a common fibular (peroneal) nerve palsy:
The isolated loss of ankle eversion and dorsiflexion are most consistent with a common fibular nerve palsy. Loss of inversion and sensory disturbance in addition would suggest an L5 root lesion.
94
What is the tetrad seen in Wernicke's encephalopathy?
Confusion, ataxia, nystagmus and opthalmoplegia.
95
What happens if Wernicke's encephalopathy is left untreated.
Left untreated, the condition can progress to Korsakoff's syndrome. This syndrome affects the mammillary bodies to cause irreversible deficits in anterograde and retrograde memory.
96
Issues with phenytoin:
Need to be very careful with the dose and requires cardiac monitoring.
97
Definition of SE:
Seizure lasting more than 5 minutes or multiple seizures lasting more than 5 mins without ROC.
98
Summarise the key features of temporal arteritis:
Temporal arteritis (also known as giant cell arteritis: GCA) is a vasculitis of unknown cause that affects medium and large-sized vessels arteries. It occurs in those over 50 years old, with a peak incidence in patients who are in their 70s.
It requires early recognition and treatment to minimize the risk of complications such as permanent loss of vision. Hence, when temporal arteritis is suspected, treatment must be started promptly with high-dose prednisolone as well as urgent referral for assessment by a specialist.
There is an overlap between temporal arteritis and polymyalgia rheumatica (PMR) - around 50% of patients will have features of PMR.
99
Features of temporal arteritis:
- typically patient > 60 years old
- usually rapid onset (e.g. < 1 month)
- headache (found in 85%)
- jaw claudication (65%)
- tender, palpable temporal artery
- around 50% have features of PMR: aching, morning stiffness in proximal limb muscles (not weakness)
- also lethargy, depression, low-grade fever, anorexia, night sweats.
100
What investigations are carried out for temporal arteritis?
- raised inflammatory markers
- ESR > 50 mm/hr (note ESR < 30 in 10% of patients)
- CRP may also be elevated
- temporal artery biopsy
- skip lesions may be present
- note creatine kinase and EMG normal
101
Summarise the three treatment principles for treating temporal arteritis:
1. High dose prednisolone
2. Referral to ophthalmology (urgent same day as visual damage is irreversible).
3. Bone protection with bisphosphonates is required as long, tapering the course of steroids is required.
102
Summarise trigeminal neuralgia and it common causes:
Trigeminal neuralgia is a pain syndrome characterised by severe unilateral pain. The vast majority of cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems may occur.
103
Red flag symptoms in trigeminal neuralgia:
- Sensory changes
- Deafness or other ear problems
- History of the skin or oral lesions that could spread perineurally
- Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
- Optic neuritis
- A family history of multiple sclerosis
- Age of onset before 40 years
104
Diagnosis and investigations carried out for trigeminal neuralgia:
Clinical diagnosis. Can consider an MRI head to look for nerve compression if needed.
105
Trigeminal neuralgia managment:
- carbamazepine is first-line
- failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology
106
Differentials of a subarachnoid haemorrhage:
▪ Subarachnoid haemorrhage
▪ Other intracranial hhge incl
pituitary apoplexy
▪ Dissection of cerebral blood
vessels
▪ Cerebral vasculitis
▪ Reversible cerebral
vasoconstriction syndromes
▪ Cerebral venous sinus thrombosis
▪ Idiopathic
107
▪ Raised temperature
▪ Neck stiffness
▪ Seizures
▪ Alteration in consciousness
Differentials:
CNS Infection:
▪ Meningitis- bacterial , viral
▪ Encephalitis- seizures , alteration in consciousness
▪ Cerebral Abscess
▪ Subdural empyema
▪ Paraspinal collections
▪ Unusual organisms
▪ Systemic infection can also cause associated headache
108
What are the investigations carried out in a suspected CNS infection?
▪ Start antibiotics/ antivirals
▪ CT Brain
▪ DO NOT delay an LP if no contraindications
▪ MR brain in encephalitis –temporal lobe changes /
hhge
109
Raised ICP features:
▪ Headaches worsening on lying down or waking a patient from sleep
▪ Brought on by Valsalva
▪ Visual obscurations- maybe accompanied by pulsatile tinnitus
▪ Papilloedema
▪ Diplopia from a 4th or 6th nerve palsy
110
Differentials of a headache with features of a raised ICP:
▪ Tumours
▪ Cerebral venous sinus thrombosis
▪ Malignant meningitis
▪ Significant Chiari malformation
111
Features of IIH:
Classical clinical features include headache and visual disturbance.
The headache is classically non-pulsatile, bilateral, and worse in the morning (after lying down or bending forwards).
112
Treatment summary for IIH:
First line management of idiopathic intracranial hypertension (and the only intervention supported by good evidence) is weight loss.
Failing this, patients often try carbonic anhydrase inhibitors, such as acetazolamide, but its extensive profile of side effects (peripheral paraesthesia, anorexia and metallic dysgeusia) mean that it is poorly tolerated.
Topiramate is also commonly used for headache prophylaxis.
More invasive strategies to lower CSF pressure including therapeutic lumbar punctures and surgical CSF shunting are tried in resistant cases.
In patients with prominent visual symptoms (but otherwise manageable headaches), optic nerve sheath fenestration may protect against visual loss.
113
Essential investigations for headaches with raised ICP features:
▪ CT brain+ contrast and
venogram
OR
▪ MRI brain and venogram
114
Temporal arteritis summary:
– Jaw claudication
– Stroke like features
– Raised infl markers
– Along with starting steroids a temporal
artery biopsy has to be arranged to happen
as early as possible ( preferably within 48
hours- 7 days )
115
Diagnostic criteria for episodic migraine:
▪ Diagnostic criteria:
▪ A. At least 5 attacks fulfilling criteria B–D
▪ B. Headache attacks lasting 4–72 hours (untreated or unsuccessfully treated)
▪ C. Headache has at least two of the following characteristics:
– 1. unilateral location
– 2. pulsating quality
– 3. moderate or severe pain intensity
– 4. aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)
▪ D. During headache at least one of the following:
– 1. nausea and/or vomiting
– 2. photophobia and phonophobia
▪ E. Not attributed to another disorder
116
What causes the aura in a migraine?
Under functioning of the cerebral cortex.
117
Forehead sparing stroke vs bell's palsy
Stroke spares
Bell's palsy includes paralysis of the forehead
118
What is meant by ophthalmoplegia?
Ophthalmoplegia, also called extraocular muscle palsy, paralysis of the extraocular muscles that control the movements of the eye. Ophthalmoplegia usually involves the third (oculomotor), fourth (trochlear), or sixth (abducens) cranial nerves. Double vision is the characteristic symptom in all three cases.
119
Anterograde vs retrograde memory loss:
Anterograde: This kind of memory loss means you can't form new memories. This word partly comes from the Latin word “ante,” which means before. In this context, a person can't store memories moving forward. Retrograde: This kind of memory loss means you lose memories from your past.
120
What serious complication to be aware of with patients on lamotrigine?
Development of a rash - SJS!!
121
What are category 1 anti-epileptics?
Give two examples:
Anti-epileptics that require you to stay on the same brand.
- Phenytoin and carbamazepine.
122
Risk of a patient with epilepsy taking tramadol?
Lowers seizure threshold.
Ciprofloxacin does this too.
123
What is the only medication licensed to treat MND?
Riluzole is the only medication licensed for the treatment of motor neuron disease, and extends life expectancy by around three months
124
Explain the use of thrombolysis for stroke.
Thrombolysis is the definitive treatment in a patient with ischaemic stroke confirmed by CT head scan who has presented sooner than 4.5 hours after symptom onset.
125
What antibodies are most commonly seen in MG patients?
Antibodies to post-synaptic acetylcholine receptors (Anti-AChR)
126
Explain the surgical management of mystasthenia gravis.
Surgical management with thymectomy is considered in some patients. Myasthenia gravis is associated with thymic hyperplasia (65% of patients) and thymoma (12% of patients). Evidence suggests thymectomy leads to symptom improvement in 50% of patients and remission in 25% of patients.
127
What scoring system is used to quantify the risk of stroke?
CHA2DS2VASc
128
Explain the CHA2DS2VASc score system:
C - Congestive Heart Failure
H - Hypertension
A - >75 years (Scores 2)
D - Diabetes
S - Previous stroke/TIA (Scores 2)
V - Vascular disease
A - 65-74 years
Sc - Sex (Female scores 1).
A score of 0 indicates low risk and anticoagulation may not be considered. A score of 1 indicates low-moderate risk and anticoagulation should be considered. A score of greater than 2 indicated high risk and anticoagulation should be started when weighed against bleeding risk.
129
What is the clinical triad seen in optic neuritis:
1. Visual loss
2. Periocular
3. Dyschromatopsia
130
What is the reversal agent for dabigatran?
Idarucizumab
131
What is the genetic cause of Friedreich's ataxia
This is caused by a triple repeat in the FXN gene encoding the frataxin protein.
Trinucleotide repeat disorder.
132
Signs of a cerebellar stroke
DANISH
133
Surgical clipping treats what brain bleed?
Subarachnoid haemorrhage
134
Surgical treatment for EDH:
Craniotomy + evacuation
Ligation of the bleeding artery may stem the blood flow and prevent the haemorrhage from worsening or reoccurring
135
Treatment for patients with acute ischaemic stroke with large vessel occlusion?
Thrombectomy
136
Endovascular coiling is a surgical intervention to treat what?
Subarachnoid haemorrhage
137
Summary of a posterior circulation stroke:
This can present with vertigo, ataxia and dysarthria due to involvement of the vestibular and cerebellar systems.
If he is within the 4.5h window, alteplase should be rapidly administered, in the absence of contraindications. CT head must be performed beforehand to rule out a haemorrhage
138
Most common thromboembolic stroke?
MCA - middle cerebral artery
139
Initial investigation for SAH
NON-CONTRAST CT
140
CT findings for hemorrhagic stroke:
Haemorrhagic stroke: HYPER-dense area on CT
141
CT findings for ischaemic stroke:
Ischaemic stroke: HYPO-dense area on CT
142
How to differentiate L5 radiculopathy with foot drop:
The main differentiating factor between L5 radiculopathy and common peroneal nerve palsy is still being able to invert the foot in common peroneal nerve palsy. It presents as a foot drop, foot eversion weakness and sensory loss to the lateral aspect of the thigh.
143
What information is carried in the dorsal column?
The sensory modalities of fine touch (tactile sensation), vibration and proprioception.
144
Where does the dorsal column deccusate?
Medulla oblongata
145
What information is carried in the anterior spinothalamic tract?
Anterior spinothalamic tract – carries the sensory modalities of crude touch and pressure.
146
What information is carried in the lateral spinothalamic tract?
Lateral spinothalamic tract – carries the sensory modalities of pain and temperature.
147
Where does decussation occur in the spinothalamic tract occur?
Spinal cord (first order neurones enter the spinal cord, ascend 1-2 vertebral levels, and synapse at the tip of the dorsal horn and decussate across the spinal cord).
148
Features of SAH:
Thunderclap
Syncope
Vomitting
Neurological weakness
Ophthalmoplegia
Neck stiffness
149
Indications of headache due to raised ICP:
Worse when lying / waking from sleep
Brought on by valsalva
Pulsatile tinnitus
Papilloedema
Diplopia (due to 4th or 6th nerve palsy)
150
What is normal csf pressure?
<25cm
151
When to consider IIH?
– Diagnosis of exclusion
– Only to be considered in the appropriate population of patients
– Papilloedema
– Ophthalmology assessment with fields
– Normal CT or MR brain and venogram
– LP - CSF opening pressure measured in the relaxed decubitus position is > 25 cm
– CSF analysis normal
152
Investigations for headache with raised ICP features:
▪ CT brain+ contrast and
venogram
OR
▪ MRI brain and venogram
153
Describe MS in 5 words!
Multifocal UMN disorder
154
Symptoms of cerebral venous sinus thrombosis:
Headache, seizure, papilloedema, reduced GCS, focal deficit.
Headache 82%
Reduced GCS 31%
Papilloedema 50%
Cranial nerve palsies 11% (II- VII)
Seizure(s) 42%
Bilateral cortical signs 4%
Focal deficit 41%
Cerebellar signs 3%
155
Investigations for cerebral venous sinus thrombosis:
CTV or MRI Venogram
156
What is meant by an orthostatic headache?
Headache onset within 5- 15 minutes of sitting up or standing up severe ( very often throbbing ) bilateral severe headache which is incapacitating.
Can occur spontaneously or due to LP.
Note the positional element is lost in chronic cases.
157
Managment of a secondary headache due to low CSF pressure:
▪ Lie flat (complete recovery is 1-2 weeks).
▪ IV fluids 8 hourly or 2-3 litres of oral fluids/ 24 hours
▪ Takes a good 1-2 weeks to recover fully
▪ In the spontaneous type- MR brain with contrast
▪ If patients are worsening despite medical treatment for 72 hours –epidural blood patch
158
Jaw claudication is highly suggestive of...
Temporal arteritis
159
Summary of Temporal arteritis:
Features, inv, and managment.
– Jaw claudication
– Stroke like features
– Raised infl markers
– Along with starting steroids a temporal artery biopsy has to be arranged to happen as early as possible ( preferably within 48 hours- 7 days )
160
Headaches red flags
– New neurological deficit
– Immunocompromised
– Known malignancy
– Elderly
– Anticoagulated
– Pregnancy
- B symptoms
161
Diagnostic criteria for migraine:
▪ A. At least 5 attacks fulfilling criteria B–D
▪ B. Headache attacks lasting 4–72 hours (untreated or unsuccessfully treated)
▪ C. Headache has at least two of the following characteristics:
– 1. unilateral location
– 2. pulsating quality
– 3. moderate or severe pain intensity
– 4. aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)
▪ D. During headache at least one of the following:
– 1. nausea and/or vomiting
– 2. photophobia and phonophobia8
▪ E. Not attributed to another disorder
162
What medications are given to manage migraine acutely?
Triptan (e.g sumitriptan)
NSAID (ibuprofen)
Antiemetic (if needed)
163
How to importantly screen for medication overuse headache in a history:
More than 10-15 doses of medication being used a month.
164
How to identify if a patient is suffering with chronic migraine?
Duration >3months
8 days a month has features of migraine
Triggers: stress, fatigue, sleep disturbance, dehydration, hormones, missing meals.
165
Suitable prophylaxis for chronic migraine:
▪ Propranalol (20-240 mg )
▪ Amitryptiline/ Nortryptiline (10- 100 mg)
▪ Topiramate (50-200 mg)
▪ Pregabalin ( 75-600 mg )
▪ Candesartan ( 4- 16 mg )
166
What are the three main trigeminal autonomic cephalgia's?
Cluster headache
Hemicrania
SUNCT / SUNA
167
What is SUNCT?
Short lasting Unilateral Neuralgiform headache with Conjunctival Tearing
Lasts a few seconds 100's of times a day
Note: Has autonomic symptoms.
168
Frequency of attacks of hemicrania:
30 minute attacks 20 times a day
169
Features of cluster headaches:
Considered a medical emergency!
▪ Unilateral, Side locked headaches. Severe pain,
▪ Autonomic symptoms (streaming of the eye and nostril, conjunctival congestion, swelling of face eyelids )
▪ Night time attacks waking pt up from sleep usually 2-6 am
▪ Severe agitation and restlessness
▪ Periodicity
170
Cluster headache treatment:
– Sumatriptan –injection / nasal spray.
– Oxygen 15L non-rebreather
171
Cluster headache long term prevention options:
– Verapamil –likely to need high doses between 480 mg - 960 mg/day -ECG monitoring
– Topiramate
– Lithium
172
What divisions of the trigeminal nerve are affected in trigeminal neuralgia?
2 and 3
Maxillary and mandibular
173
Causes of trigeminal neuralgia:
Compression of vascular loop
Tumours
MS
(Can investigate with MRI)
174
Management of trigeminal neuralgia:
Carbamazepine (usually very responsive)
Surgery - decompression / ablation
Refer to neuro
175
How is a diagnosis of MS made?
2 attacks with objective clinical evidence.
Note: With dissemination in space and time.
176
Causes of MS:
Genetics
Vitamin D insufficiency
EBV virus (small effect)
Weight/salt/smoking
177
Summarise the epidemiology of MS:
1/750 people affected in the UK.
Risk factors: Genetics, Vitamin D deficiency, EBV virus, lifestyle.
60% of patients have relapsing and remitting MS which go onto develop secondary progressive MS.
20% don’t progress (benign MS).
15% have primary progressive MS.
178
Prognosis of MS:
5yrs reduced life expectancy. Disease of morbidity not mortality.
30yrs from onset to wheelchair on average, 13yrs in progressive MS.
179
Explain what the symptoms of MS are?
- why are they so varied?
Balance/vertigo, fatigue, bladder dysfunction, spasticity, sensory dysfunction, pain, memory problems, eye/sight problems.
- MS causes damage anywhere in the CNS and so symptoms can be very diverse.
180
Treatment of acute relapse in MS
High dose methylprednisolone 500mg
181
Summarise the approach to managing MS treatment.
1. Treat acute relapse - high dose methylprednisolone.
2. Prevent relapse - interferon / dimethyl fumarate.
3. Prevent progression - ongoing studies.
4. Neural repair? - science fiction atm.
Treat the symptoms.
182
What causes long term disability in MS?
Progression! Episodes of relapse do not necessarily lead to long term disability.
183
Encephalitis causative organism:
HSV 1
184
A patient has failure to adduct on the right side, and nystagmus in the left side.
- what's the diagnosis?
Right internuclear ophthalmoplegia
- failure to adduct the affected side and nystagmus in the contralateral side.
185
Causes of internuclear ophthalmoplegia:
- Vascular (e.g. Stroke)
- Demyelination (e.g. Multiple Sclerosis): This is more commonly bilateral
186
Medication to prevent cluster headaches:
Verapamil
187
First line treatment for trigmeminal neuralgia:
Carbamazepine
188
Treatment for carotid stenosis?
Carotid endarterectomy
189
1st line treatment for absence seizures in an 8yr boy?
Sodium valproate
190
MRI finding in encephalitis:
BILATERAL medial temporal lobe involvement.
191
1st line treatment for focal seizures:
Leviteracetam or lamotrigine.
192
How does bulbar MND present?
Early tongue involvement and bulbar symptoms.
193
What are bulbar symptoms?
Lip trembling.
Drooling – inability to swallow, saliva gathers in mouth.
Dysphonia – vocal cord paralysis results in rasping voice.
Difficulty in articulating.
Weak jaw, facial muscles.
Pharyngeal muscle weakness.
194
Key presenting feature of progressive muscular atrophy?
Only lower motor neuron features.
195
Key presenting feature of primary lateral sclerosis?
Only upper motor neuron features.
196
Clinical features of spinal ALS:
Classically, there is a combination of upper motor neuron and lower motor neuron signs.
Upper motor neuron signs include spasticity, hyperreflexia and upgoing plantars (though they are often down going in MND).
Lower motor neuron signs include fasciculations, and later atrophy.
Generally, the eye and sphincter muscles are spared until late in the disease course and sensory disturbance is NOT seen (and should prompt consideration of an alternative diagnosis).
197
What key features does Brown-sequard syndrome present with?
- Ipsilateral hemiplegia
- Ipsilateral loss of proprioception and vibration
- Contralateral loss of pain and temperature sensation
Caused by hemisection of the spinal cord.
198
DANISH
Cerebellar dysfunction:
Dysdiadochokinesia (inability to perform rapid alternating movements)
Ataxia
Nystagmus (typically multidirectional)
Intention tremor (tremor during voluntary movement illustrated by the finger-nose test)
Slurred speech
Hypotonia
199
Medication to manage chorea in Huntington's patients?
Tetrabenazine
200
Side effects of topiramate:
Weight loss
Renal stones
Cognitive and behaviour changes
Teratogenic
201
Parkinsonism and vertical gaze palsy =
Progressive supranuclear palsy
202
Most common visual field defect in MS:
This patient's background of multiple sclerosis and presentation of peri-orbital pain and vision loss is highly suggestive of optic neuritis. Although optic neuritis can present with various visual field defects, a central scotoma is the most common.
203
Timeline for thrombolysing a stroke patient:
Thrombolysis is the definitive treatment in a patient with ischaemic stroke who has presented sooner than 4.5 hours after symptom onset.
204
Imaging for myasthenia gravis:
CT Chest
Myasthenia gravis is strongly associated with abnormalities of the thymus, and imaging to look for thymic hyperplasia or thymoma is warranted to evaluate the role of thymectomy
205
Presentation of Wernicke's:
Wernicke's often presents with an alcohol history along with a triad of confusion, ataxia, and ophthalmoplegia. Sometimes, there can be postural hypotension or hypothermia too
206
Why can you invert the foot in a common peroneal nerve palsy?
Inversion is controlled by tibialis posterior and anterior which is innervated by the tibial nerve.
207
What histopathological feature is seen in Parkinson's disease?
Lewy body depositions with alpha synuclein protein.
208
What histopathological feature is seen in Parkinson's disease?
Lewy body depositions with alpha synuclein protein.
209
Motor features of Parkinson's:
Bradykinesia, asymmetric resting tremor, rigidity, postural instability.
Shuffling gait, reduced facial expression, reduced arm swing.
210
Non-motor features of Parkinson's:
Constipation, depression, psychosis, ED, REM behavioural disorders, cognitive decline, anosmia.
211
Positive muscle-specific tyrosine kinase antibodies are seen in what condition?
Myasthenia Gravis
212
A saccular aneurysm is associated with what type of brain bleed?
SAH
213
What are the features of multiple system atrophy?
Parkinsonism and early autonomic clinical features such as: postural hypotension, incontinence, and impotence.
214
When are anticholinergics used in IPD?
Used in tremor-dominant PD.
215
Side effects of anticholinergic medications:
Dry eyes and mouth
Constipation
Urinary retention
216
How do COMT inhibitors work?
- name two commonly used.
The COMT inhibitors, tolcapone and entacapone, are a new class of Parkinson's medications.
By inhibiting the enzyme catechol-o-methyl-transferase (COMT), they prevent peripheral degradation of levodopa, allowing a higher concentration to cross the blood-brain barrier.
217
Where does deep brain stimulation stimulate in the brain to treat parkinson's?
Globus pallidus and subthalamic nucleus
218
Explain vascular/atypical parkinsonism:
Sometimes referred to as lower half parkinsonism.
- Predominant gait and postural instability.
- Poor levodopa responsiveness.
- Control cerebrovascular risk factors (smoking, high BP, DM, dyslipidaemia).
CT/MRI may show multiple infarcts.
219
Summarise Lewy body dementia:
LBD is parkinson's symptoms + cognitive symptoms within one year of motor symptoms.
-visual hallucination + fluctuating cognition.
- alpha synuclein
220
Summarise progressive supranuclear palsy:
Has features of early falls, postural instability, vertical gaze palsy.
- Rocket's sign - falling backwards on standing from a chair.
221
Summarise multiple system atrophy:
Parkinson's features but characterised with autonomic dysfunction (impotence is an early sign in males).
- Features of ataxia plus parkinsonism.
- Feautres of orthostatic hypotension which is managed with high salt diet, midodrine and fludrocortisone.
222
Summarise corticobasal syndrome:
Limb apraxia, dystonia (cramps), myoclonus.
- Marked asymmetry at onset.
- Cognitive deficits: Visuospatial, acalculia (can't process numbers), alien limb phenomenon.
- Cortical atrophy.
223
Differentials of Parkinsons:
PSP (LBD, vascular parkinsonism, drug induced, progressive supranuclear palsy, MSA).
Encephalitis
Frontal meningioma.
224
Diagnosis of parkinson's:
Clinical: Bradykinesia + one of:
Asymmetric resting tremor
Rigidity
Postural instability
225
Imaging for Parkinson's?
Only in unclear cases:
MRI to rule out other pathology e.g frontal meningioma, BG lesions, cerebellar changes).
DAT-spect (dopamine transporter scan.
Genetic testing - can aid genetic counselling.
226
Absent ankle reflex with foot drop = likely what
L5 radiculopathy
227
Postural instability, impairment of vertical gaze, parkinsonism, frontal lobe dysfunction = ???
Progressive supranuclear palsy
228
Vertical diplopia when reading in bed = what cranial nerve is affected?
Trochlear
The trochlear nerve innervates the superior oblique muscle which abducts, depresses and internally rotates the eye. Therefore the affected eye is unable to look down as easily, therefore causing vertical diplopia, worst on looking down (whilst reading).
229
1st line for generalised epilepsy
Sodium valproate
230
1st line medication for a focal seizure
Lamotrigine
231
1st line medication for a pregnant patient with epilepsy
Lamotrigine
232
What ophthalmic complication is seen in GCA?
Anterior ischaemic optic neuropathy is caused by inflammation in the posterior ciliary artery (a branch of the ophthalmic artery) which leads to occlusion and subsequent ischaemia to the head of the optic nerve.
233
What sign differentiates between organic and functional lower leg weakness?
Hoover's sign
234
What is Hoover's sign?
Hoover’s sign of leg paresis is a specific manoeuvre used to distinguish between an organic and non-organic paresis of a particular leg. This is based on the concept of synergistic contraction. If a patient is genuinely making an effort, the examiner would feel the 'normal' limb pushing downwards against their hand as the patient tries to lift the 'weak' leg. Noticing this is indicative of an underlying organic cause of the paresis. If the examiner, however, fails to feel the 'normal' limb pushing downwards as the patient tries to raise their 'weak' leg, then this is suggestive of an underlying functional weakness, also known as 'conversion disorder'.
235
Parkinson's tetrad + incontinence + orthostatic hypotension =
Multiple system atrophy
236
Wernicke's Aphasia is due to a lesion where?
Superior temporal gyrus
237
Broaca's Aphasia is due to a lesion where?
Left inferior frontal gyrus
238
Common complication of SAH (endo).
SIADH is a common consequence of subarachnoid haemorrhage.
- SIADH leads to hyponatremia and therefore symptoms of low sodium including nausea, vomiting, headaches, muscle cramps, and reduced consciousness.
239
Donepezil - is what class of drug?
acetylcholinesterase inhibitor
240
Parkinson’s medication that causes a pathological gambling/impulse control disorders
Dopamine agonists eg. bromocriptine, ropinirole, cabergoline, apomorphine
241
GCA effect on the eye and fundoscopy finding
Anterior ischemic optic neuropathy - fundoscopy typically shows a swollen pale disc and blurred margins.
242
First line tx in diabetic neuropathy?
Amitriptyline
Duloxetine
Gabapentin
Pregabalin
(Any of the above. Treatment is monotherapy so swap medications if one doesn't work).
243
How to differentiate acute vs chronic subdural brain bleeds on CT?
Chronic subdurals are hypodense (dark) compared to the substance of the brain as the blood has aged and lost density.
Acute subdurals will present as a bright hyperdense crescenteric bleed.
244
How do acute on chronic subdural bleeds appear on CT?
There is active extravasation into the clotted blood, which gives you a 'swirl' sign of dark blood surrounded by bright blood, this is an 'acute on chronic' bleed.
245
What is the earliest sign of MS?
Lethargy is a very common early symptom of multiple sclerosis.
246
SAH CT modality?
CT head WITHOUT contrast
247
What is diagnostic first line for MS?
MRI brain
248
A 72-year-old man is brought to clinic by his family. They are very concerned about his declining cognition. He was normally very well and independent until 3 months ago. He has lost no weight, has no headache but has been falling a lot. He also complains of urinary incontinence.
Hold on…
Is that the triad of urinary incontinence, gait instability and dementia?
= Normal pressure hydrocephalus
249
Management of normal pressure hydrocephalus:
Ventriculoperitoneal shunting
Around 10% of patients who have shunts experience significant complications such as seizures, infection and intracerebral haemorrhages
250
Bamford Stroke Classification:
1. Unilateral weakness, (plus/minus century deficit) .
2. Homonymous hemianopia
3. Higher cerebral dysfunction (e.g dysphasia).
Anterior circulation stroke
Note:
Total = all 3 symptoms
Partial = 2 symptoms
251
Features of an anterior circulation stroke:
1. Unilateral weakness, (plus/minus century deficit) .
2. Homonymous hemianopia
3. Higher cerebral dysfunction (e.g dysphasia).
252
Bamford Stroke Classification:
1. CN palsy + unilateral motor/sensory deficit.
2. Bilateral motor/sensory deficit.
3. Eye movement disorders.
4. Cerebellar symptoms.
5. Isolated homonymous hemianopia
Posterior circulation stroke
253
Symptoms of a posterior circulation stroke (Bamford classification).
1. CN palsy + unilateral motor/sensory deficit.
2. Bilateral motor/sensory deficit.
3. Eye movement disorders.
4. Cerebellar symptoms.
5. Isolated homonymous hemianopia (macular sparing)
254
Bamford stroke classification:
- Sensory only, motor only or sensorimotor.
Lacunar syndrome
255
Presentation of an ANTERIOR CEREBRAL ARTERY STROKE
Anterior cerebral artery stroke causes leg weakness but not face weakness or speech impairment
256
Middle cerebral artery stroke features
An infarct here would present with the upper limb being affected more than the lower limb and may have associated aphasia, which is not seen in an ACA infarct.
257
Features of a posterior cerebral artery stroke:
This presents with homonymous hemianopia with macular sparing and visual agnosia. CN affected.
258
Posterior inferior cerebellar artery stroke features:
If this artery is affected, it leads to a lateral medullary syndrome which is characterised by ipsilateral facial pain loss and temperature loss and contralateral limb/torso pain loss with temperature loss as the spinothalamic tract is affected.
Aka Wallenbergs!
259
Anterior inferior cerebellar artery (lateral pontine syndrome) stroke features:
Ipsilateral: facial paralysis and deafness
260
How does a lacunar stroke present?
present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with hypertension
common sites include the basal ganglia, thalamus and internal capsule
261
Management of autonomic dysreflexia:
Management of autonomic dysreflexia involves removal/control of the stimulus and treatment of any life-threatening hypertension and/or bradycardia.
262
Cape-like loss of pain and temperature sensation due to compression of the spinothalamic tract fibres decussating in the anterior white commissure of the spine describes what condition?
Syringomyelia
263
Side effects of SODIUM VALPROATE
Sodium = Hyponatraemia
V - VALPROATE:
A - Appetite increase --> weight gain
L - Liver failure
P - Pancreatitis
R - Reversible hair loss (alopecia)
O - Oedema
A - Ataxia
T - Teratogenic, tremor, thrombocytopaenia
E - Enzyme inducer (p450), encephalopathy (due to high ammonia)
264
Treatment for a medication overuse headache (assume patient has been overusing paracetamol, sumatriptan, codeine).
Medication overuse headache
• simple analgesia + triptans: stop abruptly
• opioid analgesia: withdraw gradually
265
Neuro complications of sinusitis:
seizure after acute sinusitis PLUS;
- Focal Neurology - Cerebral Abscess
- Cranial Nerve Palsy, Ophthalmoplegia - Cavernous Sinus Thrombosis
- Neck Stiffness, Photophobia, Kernig's/Brudzinski's positive - Meningitis
Other complications
- Painful Ophthalmoplegia, Proptosis, Eye swelling - Orbital Cellulitis
- Staph. Aureus - Associated with increased risk of frontal bone osteomyelitis
266
Seizure type with floaters and flashes
Occipital
267
Seizure type with paraesthesia
Parietal
268
Midbrain stroke characterised by the an ipsilateral CN III palsy and contralateral hemiparesis
Weber’s syndrome
269
What is seen on bloods in neuroleptic malignant syndrome?
Raised CK leukocytosis
270
How do lacunae strokes present?
unilateral motor disturbance affecting the face, arm or leg or all 3.
complete one sided sensory loss.
ataxia hemiparesis.
271
vertigo, hearing loss, tinnitus and an absent corneal reflex =
Vestibular Schwanoma
272
MS imaging
MRI WITH CONTRAST
273
Additional management after giving steroids for Bell’s palsy?
Artificial tears and taping shut the eye
274
Paralysis, low GCS, and bilateral pinpoint pupils are characteristic of what?
Pontine haemorrhage
275
Ropinirole mechanism of action:
Dopamine agonist
276
Superior homonymous quadrantanopias are caused by lesions where?
Superior homonymous quadrantanopias are caused by lesions of the inferior optic radiations in the temporal lobe.
277
How do anterior cerebral artery strokes present?
(ACA) strokes are characterised by:
Contralateral hemiparesis and sensory loss with the lower extremity being more affected than the upper.
278
How do anterior inferior cerebellar strokes present?
AICA strokes often present with sudden-onset vertigo and vomiting, ipsilateral facial paralysis, and deafness.
279
How do middle cerebral artery strokes present?
(MCA) strokes are the most common, but they would typically present with contralateral hemiparesis and sensory loss with the upper extremity being more affected than the lower, contralateral homonymous hemianopia, and aphasia.
280
What causes lateral medullary syndrome?
Lateral medullary syndrome is caused by posterior inferior cerebellar artery strokes (PICA).
281
Anterior cerebral artery stroke causes what symptoms?
Anterior cerebral artery stroke causes leg weakness but not face weakness or speech impairment.
282
Sudden onset vertigo and vomiting, ipsilateral facial paralysis and deafness - anterior inferior cerebellar artery
IPSILATERAL facial paralysis!! AICA with cerebellar signs and deafness.
283
Patients with GBS may have pain where?
Back/leg pain is seen in the majority of patients with Guillain-Barre syndrome
284
Back/leg pain is seen in the majority of patients with Guillain-Barre syndrome
Back and leg pain = make GBS a differential to rule out!!
285
Broaca’s lobe is located where?
Frontal lobe
286
Wernicke’s is located where?
Temporal lobe
287
For MS you need an MRI brain WITH CONTRAST.
- you always forget this so what type of contrast do they use for MS?
CONTRAST USED IN MS because it shows inflammation better!
Suspected optic neuritis: MRI of the brain and orbits with gadolinium contrast is the investigation of choice.
288
What differentiates Korsakoff's from Wernickes?
An inability to acquire new memories and confabulation suggests the development of Korsakoff's syndrome.
289
Always replace vitamin B12 before folate - giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord
Started on folate recently more sus of Subacute CDC!
290
Define GBS:
GBS is an ascending inflammatory demyelinating polyneuropathy that presents with lower motor neurone signs affecting the lower limbs.
291
Hemicrania continua tx
Indomethacin
292
Which anti-epileptic is most associated with weight gain?
Sodium valproate may cause weight gain
293
Carbamazepine to treat what...
Trigeminal neuralgia
294
Treatment of NEAD
1. Trauma therapy / General CBT
2. Treatment for mood disturbance / anxiety.
295
Define tetraparesis
Weakness in all four limbs aka quadraparesis
Paresis = weak
Plegia = paralysis
296
Inv for GBS
Spirometry FVC!
ABG - T2 resp failure?
LP shows raised protein, normal cell count, glucose normal
NERVE CONDUCTION STUDIES and EMG!
297
What do nerve conduction studies assess?
- used to confirm GBS diagnosis
1. Speed of impulse (slower in GBS due to demyelination)
2. Amplitude (lower in GBS)
298
GBS treatment
IVIg and plasmapharesis
299
Tetrabenazine is used for what?
To manage chorea in Huntington's patients.
300
Dimethyl fumarate is used for what?
Prevent relapse in MS
301
Syringomyelia presentations
Syringomyelia classically presents with cape-like loss of pain and temperature sensation due to compression of the spinothalamic tract fibres decussating in the anterior white commissure of the spine.
302
Investigation syringomyelia
MRI
303
What is EMG?
Electromyography - tests muscle response to an electrical impulse
304
2nd line stroke prevention is clopidogrel not tolerated:
clopidogrel is contraindicated or not tolerated, give aspirin and modified release dipyramidole for secondary prevention following stroke
305
What is meant by the munro kelli doctrine?
Blood flow to the brain is directly proportional to the resistance in the arteries and inversely proportional to the blood pressure.
306
CPP = (Neuro theme)
CPP (Cerebral perfusion pressure) = MAP - ICP.
307
The standard HbA1c target in type 2 diabetes mellitus is what?
48 mmol/mol
308
Recent travel abroad: Splenomegaly, Spots, Slow HR
Typhoid fever
