Neurology FC Flashcards
what are the two types of stroke?
ischaemic or haemorrhagic
describe a stroke
A clinical syndrome consisting of rapidly deteriorating clinical signs
focal or global disturbance lasting over 24 hours or leading to death
no other apparent cause other than that vascular origin
what two things can lead to an ischaemic stroke
vascular occlusion or stenosis causing a decrease in blood flow
what are the causes of vascular occlusion which leads to ischaemic stroke
large artery atherosclerosis causing thrombus formation
small vessel (lacunar) thrombosis
cardio embolism venous thrombosis vasculitis
sickle-cell anaemia
hyper- coagulated state
what are the risk factors of ischaemic stroke
over 55 past medical history of TIA or ischaemic stroke hypertension smoking diabetes mellitus atrial fibrillation carotid stenosis
what areas of the brain does the anterior cerebrum artery supply
part of the frontal lobe
- motor cortex sensory cortex
part of the parietal lobe
what areas of the brain does the middle cerebral artery supply
lateral aspect of the frontal lobe
- part of the motor cortex and sensory cortex
part of the parietal lobe
part of the temporal lobe
what part of the brain does the posterior cerebral artery supply
the occipital lobe
some of the temporal lobe
some of the parietal lobe
what is a function of the frontal lobe
executive functions thinking planning organising problem-solving emotions and behavioural control/personality
what is a function of the parietal lobe
perception
making sense of the world
arithmetic
spelling
what is the function of the temporal lobe
memory understanding, language
what are two quick toolkits that can assess the risk of symptoms being caused by stroke
FAST + ROSIER
describe the presentation of stroke
anonymous Hemienopia/transient visual defects aphasia ataxia dysarthria
what visual defect is classic for a stroke involving the posterior cerebral artery
diplopia
what visual defect is a classic sign for a stroke involving the anterior cerebral artery
gaze paresis
if hemiparesis is present what type of stroke causes indicate
lacunar
what must you exclude in the diagnosis of a stroke
hypoglycaemia
what is the key window of time between onset of symptoms and management in a stroke
four and 1/2 hours so urgent admission in less than four hours is required
what investigation should you order promptly when arriving to hospital with a patient with suspected stroke
non-contrast CT (due within one hour of admission)
what are the criteria for ordering a non-contrast to CT in a ?stroke
patient on anticoagulation indications for thrombolysis bleeding tendency GCS <13 unexplained progressive or fluctuating symptoms severe headache at onset of stroke symptoms papilloedema neck stiffness or fever
why does a normal CT scan not rule out stroke
particularly in the first few hours CT scan can be normal or show very subtle changes of ischaemia
in a patient with ?stroke what should be done if GCS is rapidly decreasing or is <8
endotracheal intubation
what should the target oxygen be in a patient with ?stroke
~96% give oxygen only asserts less than 95%
what is the first-line treatment of an ischaemic stroke if caught within 4/2 hours
I V altepase
why is it tight glycaemic control important in the management of stroke
hyperglycaemia is associated with intracranial bleeding and poor outcomes
would you give antihypertensive medication to individuals with ?stroke
only if they are in a hypertensive crisis such as hypertensive encephalopathy hypertensive neuropathy hypertensive cardiac failure/myocardial infarction aortic to section pre-eclampsia/eclampsia
what continuous checking should you perform in a patient with an ischaemic stroke
BMs, 12hr ECG for AF and monitoring ICP
if a ?stroke patients ICP is increasing what should you do
repeat CT
what are the indications for urgent referral to neurosurgery
large MCA or cerebellar impactsor PCA or if thrombolysis is contraindicated
what is the ongoing management of stroke
aspirin or an antiplatelet
what is the most common reason for haemorrhagic stroke
cerebrovascular changes induced by hypertension
what are the causes of haemorrhagic stroke
uncontrolled hypertension cerebral amyloid angiopathy (this is one of the few primary non-hypertensive causes) anticoagulant associated haemorrhage cerebrally infarct also rebuild tumour brain AVM cocaine and amphetamine drug abuse
what are the symptoms of a haemorrhagic stroke
headache (either insidious or thunderclap) sudden onset which progressively worsens neurological symptoms depend on the location of the bleed but are very similar to that of an ischaemic stroke
what features in a patient’s history would indicate a subarachnoid haemorrhage/haemorrhagic stroke
thunderclap headache and symptoms of meningism
what as a first-line diagnostic test for haemorrhagic stroke
CT with or without angiogram - angiogram will be performed later anyway but sometimes not the first step
what blood should you perform in a haemorrhagic stroke
full blood count renal function tests clotting factors
apart from blood tests and imaging what else would you perform in a patient with ? Haemorrhagic stroke
ECG looking for ischaemic changes or arrhythmias
what is the target range of blood pressure in a haemorrhagic stroke and why is this important
160-140 // blood pressure which is too high will worsen the symptoms especially in subarachnoid haemorrhage so you wouldn’t want to lower the blood pressure but still maintains cerebral perfusion
a patient presents with a haemorrhagic stroke when you monitor their ICP rapidly increases what does this indicate
acute hydrocephalus
what is the management of an acute hydrocephalus
external ventriculostomy
what is management of raised ICP
analgesia and sedation external drainage mannitol or hypertonic saline neuromuscular blockade and deep sedation high-dose barbiturates nb. In causes of increased ICP that aren’t of inflammatory nature such as a tumour or infection corticosteroids are not useful
what are the indications for neurosurgery in the management of a haemorrhagic stroke
de-compensating or becoming clinically unstable or has a large bleed greater than 3 cm
patients are not surgical candidates what is the management of a haemorrhagic stroke
hydration and nutrition
what is a TIA
transient episode of neurological dysfunction caused by focal brain spinal or retinal ischaemia without acute infarction lasting from the minutes to 24 hours but never more than 24 hours
what scoring system can help establish if thrombosis is necessary
NIHSS – National Institutes of Health Stroke Scale
what is the main indication that the TIA has occurred not/
most TIAs already have a score which is decreasing within an hour of onset of symptoms (ROSIER score)
what is the initial management of a TIA
loading dose of aspirin
is CT required in TIA
no because the changes on TIA are so small CT cannot pick up
what investigations should be performed in a TIA
FBC PTT+INR fasting lipid electrolytes glucose ECG (trying to find any causes)
what is the management of a TIA
after initial loading dose of aspirin referred to a TIA clinic within 24 hours and then start statin as soon as TIA has been confirmed
why is referral to a TIA clinic within the next 24 hours important
risk of stroke is very high within the 10 days following TIA
what is amourisis fougax
a temporary painless loss of vision in one or both eyes
what are the causes of amourisis fougax
embolus (carotid atherosclerosis GCA vasculitis) anything which blocks the retinal ophthalmic or ciliary artery ocular causes (blepharitis iritis conjunctivitis) neurological conditions (optic new writers papilloedema MS migraine tumour) TIA and stroke
how would you investigate amourisis fougax
usually investigation depends on what other symptoms are accompanying amourisis fougax
what would be the management of anything atherosclerotic in amourisis fougax
aspirin
what is a subdural haematoma
a collection of blood between the juror and the arachnoid matter
describe the layers of the brain
insert image here
what is the pathophysiology of a subdural haematoma
usually caused by trauma anything which impacts the bridging cortical veins which empty dural venous sinuses
what is the presentation of a subdural haematoma
recent trauma with loss of consciousness or decreased GCS seizures ( can have loss of bladder and bowel function) headaches nausea and vomiting confusion diminished by response motor or vertebral response decreased in GCS score
what do unequal pupils indicate
herniation
what are the signs of a basilar skull fracture
ortorrhoea / rhinorrhoea / racoon eyes
what three things should you check quickly when dealing with a sub dural haematoma
check hypoglycaemia temperature and venous blood gases (this is the deadly triad
what should you try and establish in the history of a patient with a subdural haematoma
use of aspirin or anticoagulant/antithrombotic and any history of liver or renal disease to assess platelet and coagulation factors
what is the criteria for performing a CT head scan in the patient with ? Subdural haematoma
GCS lesson 13 on initial assessment or lesson 15 at two hours after initial assessment suspected open or depressed skull fracture any sign of basal skull fracture any focal neurological deficit episode of vomiting or post-traumatic seizure
for subdural haematoma in CT
banana shaped bleed
what is the management of subdural haematoma
any haematoma greater than 10 millimetre requires surgery + medical management. Othwerwise just medical management. - prophylactic antiepileptic’s coagulopathy correction and managing ICP
what the usual causes of an extradural haematoma
trauma
why do extradural haematoma is usually occur
temporo-parietal lobe
which vessel is usually affected in an extradural haematoma
middle meningeal artery
describe the pathophysiology of extradural haematomas
an increased volume of blood strips the juror and the meninges away from the skull and have large enough compresses the brain structures and increases ICP death can occur from midline shift or tentorial herniation
what is presentation of an extradural haematoma
history of trauma with loss of consciousness or fluctuating consciousness with then a period of lucidity occurring followed by rapid deterioration loss of consciousness reduced GCS may have blown pupil and contralateral hemiparesis
what does a blown pupil indicate in an extradural haematoma
there is a cranial nerve three palsy
what the station is diagnostic of an extradural haematoma and what is the result
non-contrast CT showing lemon -shaped bleed
what is the management of an extradural haematoma
surgery is almost always required medical management is based on reducing ICP but is often used alongside surgery
what are the complications associated with extradural haematoma’s
infections if there is skull fracture ischaemia post-traumatic epilepsy cognitive impairment hemiparesis hydrocephalus brainstem injury and death
what are the two most common causes of subarachnoid haemorrhage
traumatic or from spontaneous burst of aneurysm
what is the function of the arachnoid and pia mater
the arachnoid and pia mater cover the brain service and key in protecting from intracerebral infections the arachnoid also holds arachnoid villi which absorb CSF
what is the presentation of a subarachnoid haemorrhage
thunderclap headache peaking at one – five minute lasting around one hour with associated symptoms of vomiting nausea photophobia with a reduced and falling GCS and meningism
what is the initial management of subarachnoid haemorrhage
intubate them subarachnoid haemorrhages will always require intubation eventually so into early give isotonic fluids and check pupils every 20 minutes
what investigations should be performed in a subarachnoid haemorrhage
FBC U+E LFT non-contrasted CT +/- angiogram
when is a lumbar puncture indicated in the investigation of the subarachnoid haemorrhage
from onset of symptoms
as soon as you diagnose a subarachnoid haemorrhage what is the first line management
nifedipine preventing cerebrally ischaemia
how does nifedipine prevents cerebral ischaemia
stops arterial vasospasm
if the subarachnoid haemorrhage was caused by an aneurysm what is the long-term management
aneurysm should be secured within 48 hours so-called neurosurgeon
what are some potential consequences of subarachnoid haemorrhage
re bleed or acute hydrocephalus
Describe the typical symptoms of parkinsonism
bradycardia rigidity tremor and postural instability
described the pathophysiology of Parkinson’s disease
an unknown process causes loss of dopaminergic neurons in the substantia nigra of the basal ganglia/cells in the substantia nigra degenerate and deposit proteins which formally bodies these correlates with dementia and cognitive impairment/decrease in the dopamine production causing a decreased activation of direct basal ganglia pathway thus decreasing the movement initiation/decrease of inhibition of the indirect basal ganglia pathway increases movement inhibition there is also impaired regulation of muscle tone causing hypotonia and impaired postural reflexes causing postural instability/these altered feedback loops also cause psychiatric manifestations causing anxiety and depression
describe their direct basal ganglia pathway and how it’s affected in Parkinson’s
the motor cortex releases glutamate which activates the striata (dopamine is released by the substantia nigra which also stimulates a straight him)the striatum produces a gabapentin which has inhibit treatment that affects on the globus pallida’s and the substantia nigra these produce some gabapentin which inhibits the thalamus thus allowing for increased excite a treat signals to be produced increasing muscle movement in Parkinson’s decrease in dopamine will mean that the thalamus isn’t inhibited so the thalamus in itself can inhibit excitatory signals to the motor cortex thus decreasing movement initiation
what are syndromes which mimic Parkinson’s disease
progressive super nuclear palsy multiple system atrophy Lewy body dementia corticobasal syndroma
what is the presentation of Parkinson’s disease
bradycardia resting tremor rigidity micrograph ear decreased facial expressions and hypo phony due to relax muscles and larynx cognitive decline anxiety and depression
if cognitive decline is present what does this mean about the Parkinson’s disease
it is advanced
describe the tremor associated with Parkinson’s
resting tremor usually asymmetrical at 4 – 6 Hz
describe what is meant by rigidity in Parkinson’s
Increase resistance on passive movements and cog wheeling shuffling and astute gate
if there are symptoms of Parkinson’s in anyone under the age of 40 what disease process is actually going on
Wilson’s
describe the features of Wilson’s disease and how they differ to Parkinson’s disease
Wilsons has an acute not progressive onset Wilsons has a rapid progression of the slow progression Wilsons has early cognitive involvement not late disease stage Wilsons has a symmetrical neurological deficit whereas Parkinson’s is usually asymmetrical Wilsons has upper motor neuron signs
what investigation should you perform in an individual with ?Parkinson’s disease
a trial with dopaminergic drugs if there are objective improvements then it is diagnostic any atypical presentations then you should do a MRI ( MRI also indicated if there is cognitive involvement)
describe the management of very mild Parkinson’s disease
MOAI - rasagillina dna selegine ( inhibit dopamine catabolism)
describe the management of mild Parkinson’s disease
dopamine agonist rapinirole carbidopa levodopa or anti-cholinergics
when word dopamine agonists be first line in the treatment of Parkinson’s
in over 70s
why would dopamine agonists not be first line management in individuals younger than 70
have a higher side-effect profile of dyskinesia orthostasis and hallucinations
in who wouldnt you give anti-cholinergic drugs for the treatment of Parkinson’s
in the elderly (over 65/70) as they have an increased side-effect risk
what is the management of moderate Parkinson’s disease
ad anti-cholinergic beta-blocker or DBS to dopamine agonists if symptoms are uncontrolled or if there are motor fluctuations you can try extended action dopamine agonists
nausea and vomiting is a common side effect of anti-Parkinson’s drugs what would you used to treat this
domperidone
what is meant by parkinsonian-ism plus
Parkinson’s which isn’t idiopathic and has an extra layer to it
what are the types of parkinsonian is plus
super nuclear policy called co-basal degeneration multiple system atrophy Lewy body dementia
described the presentation of super nuclear palsies in parkinsonian plus
postural instability with vertical gaze palsy symmetrical onset and truncal rigidity
what is the pathophysiology behind super nuclear palsy parkinsonian plus
TAU tangles
describe the presentation of cortical basal degeneration in parkinsonian plus
apraxia aphasia AsteroGenesis
what is the pathophysiology behind cortical basal degeneration
TAU tangles
describes the presentation of multiple system atrophy in parkinsonian-ism plus
autonomic dysfunction of postural hypotension bladder dysfunction and cerebellar signs
describe the pathophysiology behind parkinsonian plus multiple system atrophy
cell loss and gliosis
what is the most common type of parkinsonism plus
Lewy body dementia
what are the symptoms of parkinsonism plus Lewy body dementia
variation in cognition visual hallucinations rem sleep disturbances or orthostatic hypotension
what is the pathophysiology behind Louis body dementia
alpha synuclein + ubiquitin aka lewi bodies
what genetic defect causes Huntington’s disease
repetition of the CAG gene
the XXXX CAG repeats the XXXXX age of onset of symptoms
more / younger
Describe the pathophysiology of Huntington’s disease
increased to CAG repeat causes excess glutamine to be produced this causes abnormal protein cleavage and accumulations of intracellular toxic aggregates this causes both neural abnormalities from cell death and a global atrophy as well as basal ganglia atrophy and thalamic atrophy . there is also a relative access and dopamine caused by the overexpression of the CAG gene depleting the GABA neurones of the straighten causing an over activation of the indirect pathway so there is less movement inhibition
what other non-neuronal abnormalities of Huntington’s disease
death of cardiac myocytes causing cardiomyopathy and skeletal muscle atrophy
describe how chorea and athetosis occurs in Huntington’s disease
death of staiatum GABA cells means there is less GABA production thus less inhibition of the globus Pallas this means there is increased inhibition of the subsoil I make nuclei which decreases the activation of the substantia nigra and the globus pallida’s thus decreasing the inhibition on the calamitous and increasing the activation from with the laminators to the motor cortex so there is less inhibition of movements
what are the three modalities in which Huntington’s can present
movement cognition and other
describe the movement Sx of hunstingtons
Chorea twitching and restlessness Athestosis dysarthria dysphasia dystonia and weakness of muscles on prolonged contractions such as protruding the tounge
describe the cognitive manifestations of Huntington’s
changes in personal habits and hygiene disinhibition or unusually anxious behaviour depression obsessions and compulsions
what’s are the other features (apart from movement and cognitive) of Huntington’s
systolic heart failure and weight loss and muscle atrophy
what are the earliest manifestations of Huntington’s
decreased performance at school or at work
how do you manage chorea of huntingtons
tetrabenzine antipsychotics and benzodiazepines
when is tetrabenzine contraindicated
in patients with prominent behavioural problems use antipsychotics instead
drugs for chorea be lowered or stopped as disease progresses in Huntington’s
because as the disease progresses chorea decreases and rigidity increases the side effects of these drugs may actually make the chorea worse
how would you manage bradykinaesia in Huntington’s
dopamine antagonist
what nonphysical manifestation of Huntington’s should be addressed in its management
depression treat with SSRI counselling for patients and family
how do you diagnose Huntington’s disease
genetic testing looking at CAG repeat
what might you see on MRI or CT of huntingtons
caudate or striatal atrophy (only seen in late disease)
what are the differences between huntingtons and parkinsons
insert image page 16
What is the presentation of a migraine
headaches lasting four – 72 hours if untreated throbbing unilateral pain nausea and vomiting sensitivity to light aura and inability to function
what is acute management of migraine
simple analgesia plus a triptan if very nor she has add an antiemetic such as Metoclopramide
when would preventative management be given to migraine sufferers
if occurring more than once a week or when they occur they are very prolonged and severe if they are at risk of medication overuse headache such as taking analgesia something else if normal management is contraindicated or ineffective if they have uncommon migraines
what is classed as an uncommon migraine
migraine with hemiplegia or a prolonged aura
describes a stepwise treatment of preventative management of migraines
propranolol –> topyramate –> amitriptyline
if migraines are linked to the menstrual cycle what preventative management should be given
OCP to control cycle
what should the follow-up be of a migraine patient after they have started preventative therapy
follow-up after six – eight weeks and again after six – 12 months after a successful therapy has been found then consider withdrawing
What are alternative therapies that manage migraines
CBT acupuncture mindfullness riboflavin
when are riboflavins contraindicated
pregnancy
A patient presents with intense pain unilaterally around the eye/behind I and temporal area with pain lasting between 15min – 3h when these headaches occur they become restless and agitated and have watery eyes and runny nose sometimes they get nausea and vomiting with photophobia and phonophobia what is the diagnosis
Cluster headache
patient presenting with cluster headaches says that they get lacremation and rhinorrhoea What is the name given to these symptoms and what are other examples of this which can occur in cluster headaches
autonomic symptoms : partial Horner’s syndrome with ptosis and meiosis conjunctival injection facial swelling and redness
a patient presents with extremely severe pain unilaterally around the iron temporal area which has been lasting an hour and 1/2 new notice that on examination they have ptosis and meiosis what is this
partial Horner’s syndrome associated with cluster headaches
what can you tell me about the frequency of cluster headaches wonder they come on
attacks are usually psychical at the same time of day or the same time of year and occur in clusters which last seven days – one year with periods of remission in between clusters
what investigations should you perform in a patient who presents with extremely severe unilateral pain around the eye and temporal area
CT to exclude subarachnoid haemorrhage and also check for any causes secondary of cluster headaches ESR should be performed to exclude GCA
pituitary adenoma can sometimes cause cluster headaches apart from imaging what tests could you perform to exclude a pituitary adenoma
TFT LH FSH cortisol prolactin
describe the acute management of a cluster headache
sub cut injection of sumotriptan or intranasal O2 hundred percent for 15 – 20 minutes
how does the management of cluster headaches (acute) change if the patient has cardiovascular disease or uncontrolled hypertension
give intranasal Lidocaine instead of sub cut sumatriptan or oxygen therapy
what is the ongoing management of cluster headaches
high-dose corticosteroids for transitional therapy or a greater occipital nerve block
a patient presents to you saying that they have ongoing headaches which are dull occurring across all the head feel like a tight band around the head they have no associated autonomic features or aura but do experience some peri-cranial tenderness what is the most likely diagnosis
tension-type headache
what is the management of tension-type headaches
simple analgesia usually works but if they are chronic relaxation CBT and physiotherapy can help relieve symptoms
which medications can cause medicine overuse headaches
basically anything: triptan opioids NSAIDS paracetamol
what is the criteria for a medicine overuse headache
headaches occurring on 15 or more days per month if paracetamol or simple analgesia (if trip towns or opioids for combined analgesics 10 or more days) as a result of regular use of headache medication there is been the use of medication for three months or more in a person with a pre-existing headache disorder
what is the management of medicine overuse headache
explain what medicine overuse headache is that the only way to make it better is to withdraw analgesia simple analgesia and trip towns can be stopped abruptly and should be stopped for at least one month that they may experience withdrawal symptoms and symptoms may worsen initially to keep a diary of symptoms and maintain good hydration and follow-up should be given after one – two months of stopping analgesia
what other risk factors associated with medicine overuse headache
psychological comorbidities family history acquired central sensitisation neurotransmitter abnormalities (reduction 5-HT) people with an underlying headache condition women aged 40 to 45
what is a dermatome
an area of skin supplied by a single spinal nerve root and used in sensation
what is a miyotome
A group of muscles innovated by a single spinal nerve used for movement and power
shoulder shrugging describes what nerve root
C4
shoulder Abduction and external rotation as well as elbow flexion describes what nerve root
C5
wrist extension describes what nerve root
C6
elbow extension and wrist flexion describes what nerve root
C7
thumb extension and finger flexion describes what nerve root
C8
finger abduction described what nerve root
T1
hip flexion describes what nerve root
L2
knee extension describes what nerve root
L3
ankle dorsiflexion describes what nerve root
L4
big toe extension describes what nerve root
L5
ankle plantar flexion describes what nerve root
S1
bladder and rectum motor supply describes what nerve root
S4
what nerve roots are involved in the cervical plexus
C1 – C4
what does the cervical nerve plexus innervate
the diaphragm shoulders and neck
what nerve roots are involved in the brachial plexus
C5 – T1
what does the brachial plexus innovate
the upper limbs
what does the lumbosacral plexus innerate
the lower extremities
what nerve roots are involved in the lumbosacral plexus
L2 – S1
what is Multiple Sclerosis
a demyelinating inflammatory disease characterised by episodic neurological dysfunction in at least two areas of the central nervous system separated in space and time
the patient presents to you with greying or blurring of their vision and some pain when they move one of their eyes it has lasted two days and they have no other symptoms they noted that they have had similar episodes in the past but not as severe and it resolved quickly what would you be suspicious of
Multiple Sclerosis
how can Multiple Sclerosis present initially
with a history of transient motor cerebellar sensory gait or visual dysfunction periods lasting over 48 hours and are not accompanied by other intercurrent illnesses less commonly can present with onset of weakness after repetitive movements (such as walking long distances causing foot dragging) or in voluntary movements such as cramping or jerks urinary frequency or bowel dysfunction or spasticity and increased muscle tone
how can spinal-cord lesions present in Multiple Sclerosis
present with asymmetrical findings and episodes of odd sensations such as wetness or tingling they may also get band like sensations across the body
the patient presents to you with greying or blurring of their vision and some pain when they move one of their eyes it has lasted two days and they have no other symptoms they noted that they have had similar episodes in the past but not as severe and it resolved quickly what investigation should be performed in what may be found
optic neuritis showing a pale optic disc
would Multiple Sclerosis show upper motor neurone signs or lower motor neuron signs
upper motor neuron
if you suspect a patient has Multiple Sclerosis and when examining the eye movements note nystagmus what does this indicate
cerebellar dysfunction
if you suspect the patient has Multiple Sclerosis what is the diagnostic test for MS
MRI with contrast
what blood test would you want to perform to exclude differentials for Multiple Sclerosis
thyroid function tests vitamin B12 diabetes mellitus (HbA1c and blood glucose)
what are oligoclonal bands and when would they be found
in CSF analysis of a patient with MS
what are the four subtypes of Multiple Sclerosis
progressive relapsing Multiple Sclerosis secondary progressive Multiple Sclerosis primary progressive Multiple Sclerosis relapsing remitting Multiple Sclerosis
a steady decline since the onset with superimposed tax which then partially resolve what type of Multiple Sclerosis does this describe
progressive relapsing
initially has unpredictable attacks which may or may not leave permanent deficits but usually resolved to some degree followed by periods of remission then suddenly begins to have progressive decline without any periods of remission and any superimposed attacks what type of Multiple Sclerosis does this describe
secondary progressive
a steady increase in disability without attacks - what type of Multiple Sclerosis does this describe
primary progressive
unpredictable attacks which may or may not leave permanent deficits followed by periods of remission what type of Multiple Sclerosis does this describe
relapsing remitting
what is the management of an acute flare of Multiple Sclerosis
new thou prednisolone IV high-dose oral plasma exchange for patients with severe/rapidly progressing disability
what is the ongoing management of Multiple Sclerosis
symptom management and immunomodulators such as interferon beta 1 Alpha - in relapsing remitting corticosteroids in secondary progressive monoclonal antibodies in primary progressive
patient with Multiple Sclerosis has lots of sensory symptoms such as pain what would you give to manage this
low-dose anticonvulsants such as gabapentin
a patient with Multiple Sclerosis has an increase in muscle tone what would you give to manage this
anti-spasticity medication such as baclofen clonazepam gabapentin
patient with Multiple Sclerosis has a tremor what would you give to manage this
propranolol or clonazepam
what is the pathophysiology of Multiple Sclerosis
immune system attacks the myelination of neurons this causes demyelination and is disrupts axonal supports leading to its destabilisation causing degeneration
what are signs of upper motoneuron lesions
everything goes up brisk reflexes spastic hypertonia muscle weakness babinski sign and other primitive reflexes
where do lesions commonly occur in Multiple Sclerosis
the optic nerve the brainstem basal ganglia and spinal-cord
what are the signs that lesions have occurred on the optic nerve in Multiple Sclerosis
blurred vision over days optic atrophy can cause optic neuritis
what assigns the lesions occurred on the brainstem in Multiple Sclerosis
pyramidal weakness muscle weakness and spastic paraparesis
what are signs that lesions have occurred on the basal ganglia/cerebellum in Multiple Sclerosis
nystagmus tremor slowed movement ataxia
what are signs that lesions have occurred on the spinal-cord in Multiple Sclerosis
pins and needles muscle spasms muscle weakness odd sensations such as wetness/tingling band -like sensation
what is myasthenia gravis
a chronic autoimmune disorder of the post-synoptic membrane at the neuromuscular junction in skeletal muscles
what is the pathophysiology of myasthenia gravis
chronic autoimmune disorder of the postsynaptic membrane at the neuromuscular junction in skeletal muscles
a patient presents with diplopia ptosis with pupils sparing which gets worse as the day goes on what could this be
myasthenia gravis with ocular presentation
in which three modalities can myasthenia gravis present
ocular oropharyngeal generalised
what are oropharyngeal symptoms of myasthenia Gravis
dysphagia with difficulties chewing dysarthria nasal or slurred speech
a patient presents with diplopia and ptosis but pupils bearing some dysphasia you note that they have a flattened or transverse smile and on examination they have proximal with limb weakness with difficulty getting in and out of chairs they tell you that they have trouble also climbing the stairs in their home however there is no evident muscle wasting and reflexes and normal with sensation intact - what could be the diagnosis
myasthenia Gravis
if a patient with myasthenia Gravis has wasting of muscles what does this mean
they have anti MuSK antibodies
how does anti MuSK myasthenia Gravis differ from normal myasthenia Gravis
the presentation of M US K is more severe has severe facial weakness and atrophy of the face and tongue has a muscle wasting of muscles of the legs and back has a predominant neck and respiratory muscle weakness with frequent progression Myesthenia Gravis crisis also has a poor response to cholinesterase inhibitor therapy
what investigations should be performed in a patient which is ? Myasthenia Gravis
anti-cholinesterase receptor antibody assay MuSK Ab assey CT of chest
why would you want to perform a CT chest in a newly diagnosed patient of myesthenia Gravis
to exclude thymoma or thymac hyperplasia
what should you do if serological testing is unremarkable in a patient with? myasthenir Gravis
repetitive nerve stimulation testing
describe the stepwise management of myasthenia Gravis
pyridostigmine –> add in corticosteroids or immunosuppressants such as prednisolone or azathioprine do Simek to me if indicated –> add plasma exchange or IVIG –> rituximab –> . Estate mean with immunosuppressants and intermittent IVIG
what is a myasthenic crisis
is a complication of myasthenia gravis and a medical emergency it’s an exacerbation causing no respiratory drive
what is the management of myasthenia Gravis crisis
mechanical ventilation plasma exchange or IVIG with adjacent corticosteroids (second line rutiximab) you can also add in galantamine or pyridostigmine
what is the management of myasthenic crisis post crisis
intermittent IVIG
what is the basis for intubation in a myasthenic risis
low forced vital capacity and low negative in spiritual force you should not wait for an AVG as acidosis occurs late in the clinical decompensation should have a high level of suspicion
what are the triggers of an MG crisis
infection aspiration high-dose corticosteroids surgery drug reactions in contraindicated medication failure to comply with medication some cancer therapy trauma
what type of drug is galantamine
anti-cholinesterase
what type of drug is pyridostigmine
cholinesterase inhibitor
described the difference in pathophysiology between MG and LEMS
the function of the presynaptic voltage-gated calcium channels is impaired by autoantibodies resulting in the impaired ACH release rather than the destruction of ACH receptors
describes the distribution of MG and LEMS
MG: crania bulbar LEMS: largely truncal
describe the fluctuations in MG and LEMS
MG: worse after exertion LEMS: better after exertion
describe whether MG + LEMS are somatic versus autonomic
MG: somatic LEMS: somatic + autonomic
describe the presence of reflexes in MG and LEMS
MG: present even in fatigue LEMS: absent but restore
describe the result of the 1Tensilon test in MG and LEMS
MG: positive LEMS: negative
which antibodies are present in MG?
Anti nAChR + sometimes anti MSK
which antibodies are present in LEMS?
Anti VGCC
what diseases are associated with myasthenia gravis
thymic or autoimmune disease
what diseases are associated withLEMS?
cancer mostly S CLC
what is Duchenne muscular dystrophy
a progressive generalised muscular disease causing the breakdown of muscle with most patients losing the ability to walk by 12 years and requiring ventilatory support by 25
describe the pathophysiology of Duchenne muscular dystrophy
there is absence of the glycoprotein dystrophin distribution provides skeletal structural stability to the skeletal cell membrane without dystrophin there is ongoing cell membrane depolarisation due to calcium entering the cell this in turn causes degeneration and regeneration of muscle fibres however degeneration occurring much faster so muscle fibres undergo necrosis muscle cell proteins are then replaced by adipose and connective tissue causing the muscle to progressively weaken
which other areas apart from skeletal muscle does Duchenne muscular dystrophy affect and how
affects the brain and smooth muscle cells causing increased processing time reviewing lower intelligence and causing cardiomyopathy and prolonged intestinal transit
parent comes to you with the child they are worried because they are having delayed motor milestones you notes that there is calf hypertrophy and proximal hip girdle muscle weakness causing a strange gait what could be the diagnosis
Duchenne muscular dystrophy
how can Duchenne muscular dystrophy present at birth
are floppy hypotonic baby this is uncommon
how does Duchenne muscular dystrophy manifest in children
there is an imbalance of strength with flexors being stronger than extensors at all lower extremity pivots causing growers sign and muscular tenderness contractures
describe growers sign in Duchenne muscular dystrophy
the patient climbs up their body to come to a stand
what do muscular tenderness contractures cause in children with Duchenne muscular dystrophy
lumbar lordosis and heel cord contracture causing patients to walk on their toes with a wide based modelling unstable gait
a patient presents with their child who has lordosis and walks on their toes causing a wide base waddling unstable gate you note that there is some heel cord contracture and when the child wants to come to stand they have to climb up the body on examination reflexes are diminished muscle tone is diminished but sensation is preserved what is the diagnosis
Duchenne muscular dystrophy
what behavioural changes do children with Duchenne muscular dystrophy show
hyperactive with attention deficit and learning disorders
how would you diagnose Duchenne muscular dystrophy
creatinine kinase is a first-line investigation this is normally very elevated once this has been found DNA analysis is performed which is diagnostic
what is the management of a child with Duchenne muscular dystrophy who is ambulatory
corticosteroid physiotherapy exercise and psychological support
what is the management of a child with Duchenne muscular dystrophy who is a non-ambulatory
supportive therapy trying to maintain activities of daily living using aids such as wheelchairs and psychological support
what is the management of a child with Duchenne muscular dystrophy who needs ventilation
ventilation of IP PV to support inspiration muscles
what complications can occur in Duchenne muscular dystrophy and what is the management
muscle contractions – surgery heart failure - lisinopril malnutrition due to tachyopnea - intermittent positive pressure ventilation and nutritional supplements scoliosis over 40° - surgery
What are the five types of motor neuron disease
ALS and Merlot trophic lateral sclerosis PBP progressive bulbar palsy PP pseudo-bulbar palsy PMA progressive muscular atrophy MMA monomelic amylotrphy
describe what occurs in amylotrophic lateral sclerosis
death of voluntary muscle neurons - there is neurodegeneration characterised by the degeneration of motor neurons in the cortical brain stem in the ventral cord
describe what occurs in progressive bulbar palsy
neuron death of bulbar muscles like head and neck
describe what happens in pseudobulbar palsy
inability to control facial muscles without any neuron death
what is the general presentation of ALS
combination of upper motor neuron and lower motor neuron symptoms commonly present with limb or bulbar onset less frequently can present with respiratory onset
describe upper motor neuron signs of ALS
stiffness and poor balance spastic and unsteady gait painful muscle spasms of hyperreflexia
Describe lower motor neuron signs of ALS
difficulty arising from chairs and climbing stairs foot drop difficulty maintaining correct posture muscle atrophy
what is an early sign of ALS
thenar wasting
individual present to you with muscle twitching and pianful cramps, there is some muscle waisting and they complain that they have recently had trouble swallowing and also trouble doing up their buttons what is one of your differential diagnoses
ALS
as disease progresses what can manifest in symptoms in ALS
spastic tetra paresis dysphonia coughing and choking strained slurred speech poor respiratory drive
how do you diagnose ALS
is a clinical diagnosis of exclusion there is neural imaging of the whole spine and brain (especially if there are any signs of bulbar onset) EMG and NCS for show abnormalities a CSF analysis and HIV screen should be performed to find other causes and creatinine kinase will be raised
what is the management of ALS
rulizole + managing symptoms
how would you manage spasticity in ALS
baclofen
how to manage muscle weakness in ALS
physiotherapy
how would you manage poor inspiratory drive in ALS
non-invasive positive pressure ventilation
if a patient has significant bulbar upper motor neuron signs what compliaction can occur
abnormal affect this is called pseudobulbar affect and can be treated with amitriptyline
what is encephalopathy
inflammation of the brain power and climate associated with neurological dysfunction – altered state of consciousness or focal neurological signs
which type of pathogen usually causes encephalopathy
viruses
which viruses most commonly cause encephalopathy
herpes most common and enteric viruses such as coxsackie poliovirus but really most viruses can
which bacteria can cause encephalopathy
Neisseria meningitidis syphilis listeria some strains of strep and staph TB kleibisella
what are non-infectious causes of encephalopathy
/and haemorrhage SLE vasculitis metabolic hypoglycaemic autoimmune drugs and alcohol
what are the signs and symptoms of encephalopathy
altered mental status can have focal neurological abnormalities such as hemiparesis pyramidal signs cranial nerve deficits in voluntary movements seizures and any signs of the causative agent such as fever or rash
describe the differences between meningitis and encephalitis
both usually have fever and leucocytosis encephalitis will only sometimes have meningeal irritation but will nearly always have mental status changes (meningitis slightly less often) seizures are very uncommon in meningitis but very common in encephalitis and focal neurological findings are hallmark feature of encephalitis whereas it is an advanced feature of meningitis (even then only occurs in 50%)
what should you be aware of when performing a lumbar puncture and CSF analysis in ? Encephalopathy
causative agent is only identified in 50% of cases
what investigations should you run in encephalopathy
lumbar puncture and CSF analysis plus cultures full blood count U+E blood cultures liver function test urine cultures MRI chest x-ray if signs of things like a stroke or a vasculitis look for autoantibodies and performer CT head
what is the management of encephalopathy
it is a medical emergency requiring management in ICU if you suspect a viral cause start empirical antivirals if you suspect bacterial cause start empirical antibiotics suspect fungal cause start IV fluconazole he suspect autoimmune cause give high-dose corticosteroids or immunomodulators
what is the management of viral encephalitis
IV acyclovir or ganciclovir if CMV
what is the management of encephalitis if you do not find a causative agent/ have no idication as to cause
This may include endotracheal intubation and mechanical ventilation, circulatory and electrolyte support, prevention and management of secondary bacterial infections, deep venous thrombosis prophylaxis, and gastrointestinal (ulcer) prophylaxis ICP raises give high-dose corticosteroids
define a generalised seizure
both hemispheres are involved
define a focal seizure
one part of the brain/lobe is involved
an episode of losing consciousness suddenly and then quickly regaining it occurs transiently and the individual doesn’t recognise that they have lost consciousness often looks like they are daydreaming may have poor performance in schools what type of epilepsy has this
absence seizure
very brief episode usually lasting less than 30 seconds where there is repetitive jerking movements such as headbanging what type of epilepsy is this
myoclonic
a sudden increase in muscle tone causing them to stiffen and fall what type of epilepsy is this
tonic
there is a sudden increase in tone causing a fall followed by rhythmic jerking excess saliva production may have tongue biting and incontinence lasting a few minutes
tonic-clonic
why are tonic-clonic seizures particularly dangerous
can cause irregular breathing which can lead to cyanosis
an individual has a tonic-clonic seizure they then fall into a deep sleep for several hours this is normal
yes deep sleep is a normal feature of tonic-clonic seizures
sudden reduction in tone causing an individual to become floppy and can be accompanied by jerky repetitive movements (myoclonic movements) what type of epilepsy is this
atonic
an individual begins marching and waving arms in circular motions for a transient period of time (hyperkinetic movements) what type of seizure assess
frontal lobe
when would a Jacksonian March be typical in epilepsy
in frontal lobe seizures
and individual has auditory and sensory phenomena with feelings of déjà vu they can be lipsmacking and sucking clothing at the same time what type of seizures this
temporal lobe
and individual gets periods of transient visual distortion what could this be (epilepsy)
occipital
and individual get altered sensations on one side of the body and a distorted body image at the same time this is transient what type of epilepsy is
parietal
how would you diagnose epilepsy
before EEG do a CT/MRI to exclude any causes of epilepsy as well as bloods blood glucose electrolytes toxicology to exclude other causes
if you want to distinguish between a non-epileptic events and a generalised tonic-clonic seizure 10 – 20 minutes after the seizure has ended what test could you perform
serum prolactin it is raising generalised tonic-clonic seizures accurately in 10 to 20 minutes after seizure
what are antiepileptic drugs which are used in the management of epilepsy
sodium valproate carbamazepine Lamotrigine topiramate
when would you use gabapentin in the management of epilepsy
focal epilepsy
describe what a febrile seizure
a self-limiting event occurring in afebrile child between the ages of six and five in children who do not have intracranial infections metabolic disorders or histories of febrile seizures
what febrile seizures associated with
URTI tinnitus media gastroenteritis
what are two features which are very indicative of febrile seizures
absence of managers am rapid recovery of consciousness after seizure - within 30 minutes preceding febrile illness usually at the start of the illness
what are indications for a lumbar puncture in febrile seizures
neck stiffness a maculopapular rash focal prolonged or multiple seizures occurring within 24 hours impairment of consciousness history of persistent irritability or lethargy
what is management or febrile seizure which lasts over five min
benzodiazepine
what is status epilitius
a convulsive seizure that continues for longer than five minutes or multiple seizures occurring one after the other with recovery in between
what is non-convulsive status epilepticus
changes in mental status or behaviour from baseline associated with continual seizure activity on EEG just without convulsions
in the ABCD management what should you look for in A - status epilepticus
signs of obstruction respiratory distress can have compromise from excess secretions blood vomit tongue obstruction jaw lock
which type of airway is commonly inserted in status epilepticus
nasopharyngeal
in ABCD management of status epilepticus what should you look for in step C
blood pressure pulse and temperature of peripheries and body temperature capillary refill heart sounds - at this stage trying IV access
in the ABCD management of status epilepticus what should be done in step D
blood gases blood glucose take bloods if possible check pupillary response do an AVPU
what blood should get checked for in status epilepticus
cultures a urea and electrolytes liver function tests full blood tests
in the ABCD management of status epilepticus what should be looked for in thE
assessor skin for rashes marks bruises and ? pregnancy
describe the stepwise management of status epilepticus
buccal mid as alarm or IV Lorazepam administer second dose of benzodiazepine usually IV Lorazepam call anaesthesiologist and give it phenytoin IV at this point I see is largest should be arriving to give propofol Ivy and muscle relaxants to then intubate
what are side effects of Lorazepam
bradycardia hypotension respiratory depression has less cardiorespiratory side-effects than diazepam
describe the side-effects of phenytoin
continuous blood pressure and respiratory rate monitoring is required as well as ECG monitoring as has cardiac effects which can cause arrhythmia bradycardia and heart block
what are causes of status epilepticus
nonadherence or withdrawal form and come alcohol withdrawal so you will haemorrhage drug overdose metabolic abnormalities of hyponatraemia infections hypoglycaemia hypoxaemia tumour hypothermia eclampsia
what should you do one status epilepticus has stabilised
find cause and do CT head
In which age group are primary brain tumours common
children less than 15 years old
which cancers can metastasise to the brain commonly
lung - this is the most common breast thyroid testicular renal colorectal and skin (malignant melanoma)
what is the presentation of the brain tumour
symptoms of raised intracranial pressure headaches worse in the morning decreased consciousness nausea and vomiting blurred vision and double vision focal neurological signs can be part of the presentation
what focal neurological signs are commonly associated with brain tumours
parasthesi of limbs speech disorders and dysphasia seizures and by temporal hemienopia in pituitary cancers
what other risk factors associated with brain tumours
familial syndromes such as neurofibromatosis ionising radiation and x-ray exposure immunosuppression EBV and HIV previous history of cancer
what cancers are associated with HIV
primary CNS lymphoma
what cerebellar signs can be present in brain tumours
disdidokineasi ataxia slurred speech hypoTonia intention tremor nystagmus gait abnormalities
why does blurred vision occur if there is raised intracranial pressure
because of papilloedema
why would a double vision occur in brain tumours
a paralytic squint from compression of cranial nerves
which diagnostic test is used for brain tumours
MRI with contrast of brain chest and abdomen and pelvis (especially if adult to find primary tumour) and biopsy
what should you always do before performing a lumbar puncture in cases of raised intracranial pressure
perform imaging to assess risk of coning
what blood tests are useful in assessing brain tumours
FBC U+E calcium liver function tests CRP TFT PSA ( if suspecting prostate cancer)
what is the management of brain tumours if there are seizures
give anticonvulsants and high dose dexamethasone if seizures are thought to be because of raised intracranial pressure (dexamethasone)
if after performing postural changes and giving dexamethasone the ICP is still high in a brain tumour patient what should you do
give mannitol
if hydrocephalus occurs as a side-effect of brain tumour what is the management
ventriculoperitoneal shunt
what are side effects of dexamethasone
sleep disturbances increase appetite or weight gain and GI reflux
what are side effects of radiation to the head for a brain tumour
cognitive impairment bone growth retardation hair loss nausea tissue healing problems and skin problems such as blistering and lesions
what are consequences of neurosurgery which may occur after surgery for brain tumour
paralysis seizures altered personality hydrocephalus
what are complications of chemotherapy
nausea vomiting anorexia alopecia pain nerve damage cognitive dysfunction increased susceptibility to infections headaches
what is a meningioma
slow-growing tumour the forms from the arachnoid cells found in the meninges
who typically gets meningiomas
females aged 45
is a meningioma and aggressive cancer
now it is usually benign and surgically viable and rarely metastasises
why would visual loss occur in a meningioma
from optic nerve compression
how would you diagnose a meningioma
apart from usual blood tests and imaging and angiography is often needed for diagnosis
what is a pituitary adenoma
a mostly benign brain tumour which can be functional and secrete hormones
what are some side effects of having a pituitary adenoma
Cushing’s acromegaly diabetes insipidus by temporal Henry Napier hydrocephalus hypopituitarism
a pituitary adenoma is diagnosed as a prolactinoma what medical management can be used
dopamine agonist
what is pituitary apoplexy and wonders occur
but unitary apoplexy is a sudden haemorrhage in the pituitary gland which causes a rapid increase in size of the lesion causing tissue necrosis and resulting in sudden onset of visual loss headaches and hydrocephalus it is common in individuals with pituitary adenomas
what is an acoustic neuroma
a benign tumour of the vestibulocochlear schwann cells
what is a presentation of an acoustic neuroma
gradual onset of unilateral sensorineural deafness headaches vertigo dizziness unilateral face numbness absent corneal reflex nystagmus and gait abnormalities can occur in large tumours
what causes hearing loss in acoustic neuroma
compression of the cranial nerve eight
what is a craniopharyngioma
a fairly common childhood brain tumour derived from residual cells in Rathkes patch arising in the pituitary stalk which can affect both the hypothalamus and the pituitary
what is the presentation of a cranipphyaryngioma
gross failure diabetes insipidus disorders of sexual dysfunction hydrocephalus by temporal Hemienopia pituitary insufficiency
what is a primary CNS lymphoma
a type of diffuse large B cell lymphoma
what should you test for in primary CNS lymphoma
HIV EBV check CD4 count and perform lumbar puncture and cytology
what is management of primary CNS lymphoma
methotrexate and chemotherapy with radiation and dexamethasone however has poor prognosis
what is a medulloblastoma
the most common malignant tumour in children which is highly metastatic
what is a glioma
the most common primary brain tumour in adults and includes astrocytoma glioblastoma multiforme pilocytiticastrocytoma epindymona and oligodendroglioma
what is Guilian barre syndrome
an acute inflammatory polyneuropathy which is classified according to symptoms by dividing it into axonal and demyelinating
describe the pathophysiology of Guilian barre syndrome
immune-mediated attack on Schwann cells or the myelin sheath of sensory and motor nerves this is triggered by previous infection most commonly you RTI or gastroenteritis CMV or C. jejuni
a patient presents to you withnumbness pins and needles muscle weakness pain problems with balance and co-ordination
Guilian barre syndrome
describe the progression of the muscle weakness which occurs in Guilian barre syndrome
symmetrical progressive muscle weakness affecting lower limbs first then upper extremities of distal muscles before moving to the proximal muscles
what are the features of Guilian barre syndrome
progressive symmetrical muscle weakness ,paraesthesia in feet and hands can occur before the onset of weakness pain may also proceed weakness this can mimic cord compression sinus tachycardia hypertension and can have postural hypotension as well as autonomic symptoms
which autonomic symptoms are associated with Guilian barre syndrome
urinary retention and ileus
described later symptoms of guillian barre symptoms
flaccid paralysis with areflexia blurred or double vision poorest rotary drive and dysphasia persistent and severe pain
how long does guillian barre symptoms last and how do symptoms change during this time
progressively worsens for about a month and then has a period of symptoms remaining the same before gradually recovering
what is the diagnosis of guillian barre symptoms
imaging such as MRI or CT to differentiate from spinal-cord compression CSF nerve conduction studies and anti-ganglioside antibodies
what will the CSF show in guillian barre symptoms
raised proteins
what is the management of guillian barre symptoms
plasma exchange / IVIG plus supportive management of ventilation is respiratory involvement
when our IVIG contraindicated in the management of guillian barre symptoms
renal failure or IgA deficiency
what is cavernous sinus thrombosis
formation or thrombus within the cavernous sinus which can either be septic or aseptic
where does the infectious origin usually arise in cavernous sinus thrombosis (septic type)
middle third of the face of the sinuses teeth or mouth most commonly acute sinusitis
what usually causes aseptic cavernous sinus thrombosis
thrombotic process as a result of trauma iatrogenic injuries or prothrombic conditions
a patient presents who is acutely unwell they say that they have had a unilateral headache around the eyes and back of nose they have a fever and unilateral periorbital oedema although the otherwise starting to look swollen they appear septic what is the most likely diagnosis
cavernous sinus thrombosis
what is the difference between aseptic and septic presentation of cavernous sinus thrombosis
do not demonstrate signs of meningitis or infections and appear less acutely unwell however they still have focal neurological deficits and orbital signs
describe the orbital signs associated with cavernous sinus thrombosis
unilateral periorbital oedema which spreads to the contralateral eye within 40 hours extra ocular muscle weakness causing proptosis painful ophthalmoplegia
describing why the headache associated with cavernous sinus thrombosis is unilateral and in those specific areas
because caused by pain from cranial nerve five which innovates the ophthalmic and maxillary branches of the facial nerve
why do patients with cavernous sinus thrombosis get ophthalmaplegia which is painful
due to pressure on the sixth cranial nerve
what structures are found within the cavernous sinus
insert picture
what investigations should anyone with focal neurological signs and orbital signs require immediately
contrast CT/MRI and angiography may be performed if ? Thrombotic cavernous sinus
one investigations apart from imaging are required in cavernous sinus thrombosis
full septic screen
if you suspect cavernous sinus thrombosis what is the immediate management
vancomycinwith ceftriaxone
once type of cavernous sinus thrombosis has been confirmed what is the management of both aseptic and septic cavernous sinus thrombosis
IV antibiotics anticoagulation if there is no haemorrhagic complications and surgical drainage (aseptic requires thrombin lysis supported therapy and anticoagulation unless there is haemorrhage in which case supportive therapy only)
what is the most common cause for peripheral neuropathy
diabetes
what are the most common causes of peripheral neuropathy
diabetes thyroid dysfunction vitamin B12 and B6 deficiency renal disease hepatic disease inflammatory disorders such as GBS line amyloidosis vasculitis is sarcoidosis anaemia and multiple myeloma
what test should you do to exclude multiple myeloma in the presentation of peripheral neuropathy
serum or urine immuno electrophoresis
how would you manage peripheral neuropathy caused by diabetes
glycaemic control and neuropathic pain can be treated with amitriptyline pregabalin or gabapentin
what are the treatment of neuropathic pain
amitriptyline pregabalin gabapentin
what drugs can give peripheral neuropathy
metronidazole nitrofurantoin
what signs would you see on the skin in a patient with peripheral neuropathy caused by diabetes
drive thin shiny skin which may be hyper pigmented hair loss calluses and ulcers
what is polyneuropathy
generalised disease of the peripheral nerves which is a frequent manifestation of systemic illnesses
what are the more common causes of polyneuropathy
diabetes at GBS monoclonal tomography cauda equina toxins and metabolic factors( these usually cause axonal neuropathys)
describe the classic manifestation of polyneuropathy
symmetrical numbness and paraesthesia in the feet and distal lower extremities fit the stocking and glove distribution
what are early motor symptoms associated with polyneuropathy
atrophy of the intrinsic muscles and ankle weakness
what are the autonomic features which can be associated with polyneuropathy
the autonomic nervous system may be involved resulting in changes in bowel habit sweating disturbances and orthostatic light-headedness
what is a radiculopathy
painting of the nerves at the root which can sometimes also produce pain weakness and numbness such as an sciatica
what is myelopathy
compression of spinal-cord itself symptoms are usually more severe including poor coordination trouble walking or paralysis
describe the nerve distribution of the hand
insert picture
while most common mono neuropathies of upper extremities
compression neuropathies including carpal tunnel syndrome ulnar neuropathy and radial neuropathy
what usually causes compression neuropathies
mechanical injury and trauma
where does compression usually occur which causes carpal tunnel syndrome
median nerve at the wrist
where does the compression usually occur which causes unar neuropathy
elbow
where does the compression usually occur which causes radial neuropathy for the axilla
trauma or compression of the radial nerve over the spiral groove
a patient presents with wrist drop what is the most likely diagnosis
radial palsy
the patient presents with trouble doing fine movements such as doing up buttons or using coins and there is some pain in the pinkie finger what is most likely diagnosis
ulnar palsy - all the nerves supplying the small muscles of the hand
patient presents with pain in the thumb index and middle finger which radiates down to the wrist and is worse in the morning the struggles open doors and thus found the pain is worse when texting what is most likely diagnosis
carpal tunnel
what does the presence of multiple mono neuropathies outside of a compression site suggest
vasculitis or segmental demyelination although these are rare
what are sensory manifestations of mono neuropathies
pins and needles numbness and less ability to feel pain or changes in temperature (particularly in feet burning or sharp pain usually in the feet feeling of pain from something that should not be painful such as a light touch loss of balance or coordination caused by the diminished ability to tell the position of the feet or hands
what are the motor manifestations of mono neuropathies
twitching and muscle cramps muscle weakness or paralysis thinning or wasting of muscles difficulty lifting up the front part of your foot a.k.a. foot drop or wrist drop if in the hand
what are autonomic symptoms of mono neuropathies
constipation or diarrhoea feeling sick bloated all belching low blood pressure rapid heartbeat excess sweating or lack of sweating erectile dysfunction difficulty emptying bladder loss of bowel control
when can double vision occur in a mono neuropathy
cranial nerves are used for vision
what type of neuropathy is Bell’s palsy
moral neuropathy of the facial nerve cranial nerve seven
7/2 of the forehead is unresponsive to movement what type of mono neuropathy is this
cranial nerve seven a.k.a. Bell’s palsy
the patient can’t abduct the eye (the lateral rectus muscle) what type of mono neuropathy is this
cranial nerve six
the patient can’t depress rotate or adduct their right (superior oblique) what type of mono neuropathy is this
cranial nerve for
the patient has a deviated jaw and tongue what type of mono neuropathy is this
trigeminal nerve deviated towards the lesion
a patient has ptosis of one I and it is also depressed and abducted down and out the people however is reactive what type of mono neuropathy is this
cranial nerve III
what are the most common types of cervical radiculopathy
C5 and 6, C7, C8 and T1
what do C5 and C6 do and what would a radiculopathy effect
elbow flexion and sensation in the thumb also accounting for bicep reflexes
what does C7 do and what would a radiculopathy effect
elbow extension and sensation of the middle finger also tricep reflexes
what do C8 and T1 do and what would a radiculopathy effect
movement of the hand and sensation of the middle of the hand and the forearm
what are the most common lumbar radiculopathy is
sciatica involving nerves L42S3
what does L5 innovate and what would a radiculopathy effect
dorsiflexion (standing on heels) sensation of the big toe and dorsum of foot
what does S1 innovate and what would have radiculopathy effect
plantar flexion (standing on toes) allows the sensation of the little toe and the sole and heel of the foot as well as the ankle jerk reflects
what does a radiculopathy mean
nerve root compression at the root
patient presents with sharp pain in the back and legs which may worsen with certain activities weakness or loss of reflexes of the ankle numbness of the skin and pins and needles in the legs back and bum area what is this
sciatica also known as lumbar radiculopathy
what other features of radiculopathy is
sharp pain in the Dermot home weakness or loss of reflexes in the mire tome numbness of skin pins and needles or feeling abnormal sensations such as paraesthesia in the Dermot home
what are the causes of radiculopathy
herniated discs bony spurs ossification’s spinal ligaments a.k.a. anything which causes spinal stenosis
and individual gets chest pain when walking downhill and they look down at their feet what does this indicate
cervical radiculopathy is looking down narrows the spinal canal further
what are the investigations of radiculopathy
physical exam and examinations to elicit symptoms x-ray or MRI/CT (MRI is best)
what is the management of a radiculopathy
NSAIDs and other pain medication muscle relaxant (diazepam) physiotherapy and weight loss steroid injections and surgery in severe cases
what can be used to manage chronic pain in radiculopathy is
amitriptyline
what nerve root is affected if a patient has an inability to rise upon tiptoes and inability to plantar flex
S1
what nerve roots are affected if a patient has foot drop and they are unable to Dorsey Flex
common peroneal nerve/L5
what nerve roots are affected if a patient has pins and needles and weakness of the farm and index finger as well as loss of bicep weakness/reflex
C6
one our roots are affected if a patient has middle finger weakness and pins and needles and weakness of triceps/tricep reflex loss
c7
What is hydrocephalus
buildup of fluid in the ventricles within the brain which increases the size of the ventricles and put extra pressure on the brain
who is hydrocephalus common in
infants and the elderly (over 60)
which are three ways in which hydrocephalus can occur
obstructive poor absorption overproduction
describe the pathophysiology of obstructive hydrocephalus
partial obstruction of the normal flow of CSF from one ventricle to another or from the ventricles to other spaces of the brain
describe the pathophysiology of poor absorption hydrocephalus
poor absorption from the blood vessels often related to inflammation or injury to the brain
described a pathophysiology of overproduction hydrocephalus
this is the most rare type of hydrocephalus where CSF is produced too quickly then it is absorbed
what other risk factors for hydrocephalus in newborns
abnormal development of CNS causing obstruction bleeding within the ventricles which is a complication associated with premature birth infection in the uterus such as rubella or syphilis that causes inflammation of brain tissue
while the risk factors for hydrocephalus in adults/children
lesions or tumours of the brain or spinal-cord CNS infections such as bacterial meningitis or mumps bleeding from the brain from a stroke or head injury traumatic injury to the brain
what other types of hydrocephalus
communicating non-communicating normal pressure
describe a communicating hydrocephalus
CSF can flow between ventricles but is blocked at the exit of the ventricles
describe a non-communicating hydrocephalus
also known as obstructive hydrocephalus the flow of CSF is blocked between ventricles most commonly at the aqueduct of Sylvius
where is the aqueduct of Sylvia found
between the third and fourth ventricle in the middle of the brain
describe a normal pressure hydrocephalus
a form of communicating hydrocephalus most commonly in the elderly population arising from the subarachnoid haemorrhages trauma or tumours however can also be idiopathic
what is the presentation of hydrocephalus in an infant
unusually large head rapidly increasing size of herd a bulging or tense fontanelle poor feeding poor responsiveness to touch poor growth eyes fixed downwards (some setting of the eyes)
describe the presentation of hydrocephalus in adults
headaches lethargy vomiting loss of coordination/balance loss of bladder control or frequent urge to urinate impaired vision decline in memory/concentration and other skills
what other first-line investigations in a? Hydrocephalus
ultrasound scan followed by MRI or CT no contrast
a patient presents with the loss of coordination and balance and a decline in memory concentration and other skills wonder if it is Parkinson’s disease and perform a leave a dopa challenge however there is no response to therapy what is the alternative diagnosis
hydrocephalus
what would you see if you perform a lumbar puncture in an individual with hydrocephalus
increased opening pressure and symptoms which improve after lumbar puncture
what is the treatment of hydrocephalus
shunt for endoscopic third ventriculostomy
describe the pathway of CSF
CSF flows from the lateral ventricles to the interventricular foramina to the third ventricle through three cerebral aqueduct to the fourth ventricle through the lateral and median apertures to the subarachnoid space to the arachnoid villi of the dural venous sinuses to turning to venous blood to the heart and lungs were turns to arterial blood and goes back to their respective ventricles which then secrete it
describe cerebral palsy
because of neurodevelopmental delay causing abnormalities of movement and posture and limited activity. It is non-progressive disturbance caused by injuries which occur any utero or when younger than two years old
what are the types of cerebral palsy
spastic: hemiplegia quadriplegic diplegic dyskinetic ataxic
what are the possible manifestations of cerebral palsy
reduced cognition disturb communication perceptual and sensory disturbances behavioural disturbances seizures secondary MSK problems
there is increased muscle tone and brisk reflexes with an abnormal gait which type of cerebral palsy does this describe
spastic
patient has a spastic cerebral palsy mainly affecting the arms with facial sparing what type of cerebral palsy has this
hemiplegic
patient has a spastic cerebral palsy affecting the trunk with extensor posturing and poor central tone all four limbs are equally affected what type of cerebral palsy is this
quadriplegic
what is the most common cause for or drip cerebral palsy
hypoxic ischaemic injury
patient has spastic cerebrum palsy which affects the legs and arms but legs are affected much more than the arms and hand function is relatively preserved what type of cerebral palsy with this
diplegic
what is the most common cause for diplegic cerebral palsy
periventricular brain damage
patient has chorea athetosis and dystonia - what type of cerebral palsy is this
dyskinetic
what is chorea
irregular sudden brief non-repetitive movements
what is athetosis
slow writhing movements occurring distally such as at the fingertips
what is dystonia
simultaneous contractions of extensors and flexors of the trunk causing twisting of the body
what are the main features of a tactic cerebral palsy
delayed motor developments in coordinate movements intention tremor a tactic gate
what are the most common problems which children with atonic cerebral palsy can get
feeding difficulties
speech impairment
intellectual deficit
urinary incontinence
and variable sensory or proprioception of loss
what are causes of cerebral palsy
T OR CH infections premature birth vascular incidents including thrombi from the placenta mothers with factor five Leyden causing focal lesions birth asphyxia hyperbilirubinaemia neonatal sepsis RDS intraventricular haemorrhage head injuries neonatal’s seizures early onset meningitis
what can cause birth asphyxia
instrumental delivery prolonged labour trauma placental abruption
what are the investigations for cerebral palsy
every child with an equivocal diagnosis of cerebral palsy should have an MRI of the brain
what interventions can be done early (nonpharmacological) in soluble palsy
early intervention services physiotherapy occupational therapy speech therapy family education directed at helping the child achieved developmental milestones
what is the pharmacological management of spasticity in cerebral palsy
benzodiazepines Botox phenols severe spasticity using neurosurgical procedures such as intrathecal baclofen
what is the medical management of dystonia in cerebral palsy
Carbon day or leave a doper as well as —> benzodiazepines and Botox
what is the medical management of athetosis in cerebral palsy
haloperidol pimozine
was the medical management of ataxia in cerebral palsy
clonazepam or propranolol - tremour amantadine - balance and coordination
what is Alzheimer’s disease
a chronic progressive neurodegenerative disorder characterised by global non-reversible impairment in cerebral functioning
described the pathophysiology of Alzheimer’s disease
characterised by senile amyloid plaques neuro fibrillar eat how tangles and neuronal loss leading to brain atrophy was defects in Ach synthesis at a cellular level
what are risk factors for Alzheimer’s disease
increasing age female genetic inheritance or family history Down’s syndrome hyperlipidaemia diabetes cerebrovascular disease cardiovascular disease high blood pressure obesity
if Alzheimer’s develops before the age of 65 what does this mean
it is considered a young onset dementia/early onset Alzheimer’s
describe the features associated with Alzheimer’s disease
memory loss disorientation nominal dysphasia ape of the declining activities of daily living and instrumental activities of daily living personality changes visuospatial function decline
which type of memory loss occurs early in the disease process of Alzheimer’s disease
recent memory first
how does disorientation usually present in Alzheimer’s disease
misplacing items progressing to getting lost
when does a pithy manifest in Alzheimer’s disease
is a more progressive symptom becoming passive sleeping more not wanting to perform usual activities
how do visuospatial decline manifesting Alzheimer’s disease
problems with driving or messy handwriting
what are features of advanced Alzheimer’s disease
severe gait disturbance: slow shuffling gait with stooped posture
poorly dressed
confused disorientated
low mood
terminal disease marked by rigidity and inability to walk or speak
what would an MRI show in Alzheimer’s disease
general eight trophy with the hippocampus being particularly shrunken
what are specific treatments for Alzheimer’s disease
cholinesterase inhibitors such as donezepil or rivastigmine in severe disease switch to or add in memantine ethyl aspartate inhibitor
however psychiatric manifestations of Alzheimer’s disease treated
using SSRI or atypical antipsychotics such as haloperidol
what specialist investigations can be employed for Alzheimer’s disease
FDG or PET scan CSF fluid analysis for tau or amyloid concentrations which are raised
what is Lewy body dementia
and neurodegenerative disorder with parkinsonism and progressive cognitive decline prominent executive dysfunction and visuospatial impairment
what is the difference between Parkinson’s disease and Lewy body dementia
in Parkinson’s disease more motor symptoms occur first in Lewy body dementia cognitive symptoms appear first it all depends on where Lewy bodies first deposit in the brain - base of the brain equals motor symptoms outer layers of the brain equals cognitive symptoms
a patient presents with recurrent visual hallucinations of animals cognitive fluctuations REM sleep behaviour disorders and features of parkinsonism such as resting tremor and rigidity what is the most likely diagnosis
Lewy body dementia
describe how symptoms change as Lewy body dementia progresses
gets more motor symptoms (inc. risk of aspiration)and cognitive symptoms become similar to that of Alzheimer’s disease with short-term memory loss behavioural changes and agitation and restlessness
what word an MRI show in Louis body dementia
generalised cortical atrophy with relatively preserved hippocampus
what is a specialist test for Lewy body dementia
single photo and emission CT
how can you give a definitive diagnosis of Lewy body dementia
you can’t can only be made post-mortem with pathological investigation to find Lewy bodies
what a Lewy bodies made out of
alpha synuclein
what is the pharmacological management for Lewy body dementia
carbidopa/levodopar for motor symptoms cholinesterase inhibitors - rivastigminw plus psychiatric management of atypical antipsychotics like risperidone and SSRI
described vascular dementia
are chronic progressive disease of the brain causing cognitive impairment
describe the pathophysiology of vascular dementia
reduction in blood supply to the brain due to vascular events such as stroke or haemorrhage causing loss of brain parenchyma
describes the progression of vascular dementia
in theory has a stepwise degeneration with rapid cognitive decline after each vascular event however in practice is not noticeable
a patient presents with problems planning organising and decision-making difficulties following series of steps and slowed processing of information (they have functional impairment of higher processing systems) ape with the disinhibition and poor attention with less fluent speech and reduced visuospatial skills what is this type of dementia
vascular - has very little memory loss and is not an early symptom of the dementia
what our frontal release reflexes and when would they be found
things such as grasping or georgette which are signs of frontal cognitive syndrome is usually associated with retrieval memory deficit - associated with vascular dementia
what would CT or MRI show in vascular dementia
cerebrovascular lesions
what is the management of vascular dementia
antiplatelet therapy and lifestyle modification with restricted blood pressure control and statin therapy
