Neurology Flashcards
What is Gertsmann Syndrome?
When there is a lesion (stroke, tumour, etc) in the dominant angular gyrus (part of the parietal lobe), causing a constellation of acalculia (unable to do calculations), agraphia (unable understand drawing of a number on hand), L-R disorientation, and finger agnosia.
Which lobe would a lesion be if they had isolated gait apraxia?
Frontal lobe
If a patient has resurfacing of primative reflexes (pout, glabella tap, grasp), where does it suggest there is damage?
Frontal lobe
Foster Kennedy syndrome is what?
Raised intracranial pressure, optic nerve atrophy, anosmia, and personality change from a frontal lobe lesion pressing dowen on the cribiform plate
A patient presents with alexia. Where is their lesion?
Occipital lobe
Where is the lateral geniculate nucleus?
It’s in the thalamus
What is Broca’s aphasia, and where is Broca’s region?
Broca’s region is in the dominant (usually left) frontal lobe. Leads to expressive aphasia - paucity of words.
What is Wernicke’s aphasia, and were is Wernicke’s region?
Wernicke’s regions is in the dominant (usually left) temporal lobe. Receptive aphasia. Don’t understand what is being said, or really what they are saying.
What area is impacted to create a conduction aphasia?
Conduction aphasia points to a lesion impacting the arcuate fascilus which is a tract conntecting Broca’s region in the dominant frontal lobe to Wernicke’s region in the dominant temporal lobe.
What path is taken by upper motor neuron axons (cortex to spine), and where to the decussate?
The upper motor neuron cell bodies are located in the motor cortex, which is a band of the cortex at the posterior of the frontal lobe. The axons from these cells bundle together to form the central semiovale, then the corona radiata, and then the internal capsule (still in the cerebrum, getting tighter together tas the progress down towards the spinal cord). As the internal capsule travels into the midbrain is gets a different name - Crus cerebri. Then as it moves into the pons it becomes known as the ‘Basis Pontis’. Then as it reaches the medulla it becomes known as the ‘pyramids’. At the lower part of the medulla it DECUSSATES the Finally, it enters the spinal cord and becomes known as the corticospinal tract.
What path is taken by sensory neurons resonsible for pain, temperature and crude touch? Where do they synapse and where dothey decussate?
Cell bodies start in the parietal lobe, then synapse at the thalamus. Second order sensory neurons have cell bodies in the thalamus that project to through the midbrain, pons and medulla to the spinal cord ipsilaterally - spinothalamic tract. They then decussate at the spinal level nearest to the part of the body they are going to innervate and synapse with peripheral sensory nerves in the lateral aspect of the spional cord.
Is there 1 thalmus, or 2 thalamuses?
It gets called ‘the thalamus’ (singular), but it’s actually 2 mirror image structures (one for the left brain and one for the right) with symmetry across the midline. Each lobe is a concentration of nuclei that participate in modifiying processing of language, memory, motor, sensory, arousal, and visual function. There is some amount of redundancy across the lobes. So, if nuclei involved in arousal are impacted by a lesion on
the left side of the thalamus, the nuclei on the right with the same function would prevent obtundation.
What path is taken by sensory neurons responsible for proprioception, vibration and fine (discriminitive) touch? Where do they synapse and where to they decussate?
Cell bodies start in the parital lobe, axons project to the thalamus. Second order neurons project axons through the midbrain, pons and to the medulla where they decussate. Note that this is dfferent tot her spinothalamic tract which doesn’t decussate until the spinal level. The third order sensory neurons have denditic processes that extend down through the spinal cord and exit through the dorsal aspect of the spinal cord, then have a cell body in the dorsal root ganglion. The axon then projects to the tissue.
What is the role of the anterio nuclei of the thalamus?
Language and memory function
What is the role of the lateral nuclei of the thalamus?
Motor and sensory function
What is the role of the medial nuclei of the thalamus?
Arousal and memory function
What is the role of posterior (pulvinar) nuclei of the thalamus?
Visual function
Where, classically, is a lesion located if a patient presents with hemisensory loss involving the face, upper limbs and lower limbs?
In the contralateral thalamus
What are the cerebellar hemspherical signs?
Ipsilateral:limb ataxia, dysmetria, intenion tremor, dysdiadochokinesia, nystagmus
What happens if you have lesion in your cerebellar vermis? (the medial part of the cerebellar)
Trunkal ataxia and nystagmus
What are the components of the brainstem in order?
From superior to inferior: mdibrain -> pons -> medulla
Rule of 4s: what are the cranial nerve nuclei located in the midbrain?
Cranial nerves 3 and 4. Note that nerves 1 and 2 have their nuclei in the brain itself, superior to the midbrain.
Rule of 4s: what are the four structures in the midline of the brain that begins with M?
Motor pathay (corticospinal tracs), medial lemnisus (dorsol column), medial longitudinal fasciculius, and motor CN nuclei (CN 3,4, 6, 12)
Rule of 4s: what are the four structres on the sides (lateral) of the brainstem that begin with S?
Spinocerebellar pathways, spinothalamic pathways, sensory nucleus of the 5th CN, sympathetic tract
What are the bulbar signs?
Signs and symptoms suggestive of problems with cranial nerves IX, X, XI, XII. These are the 4 cranial nerves located in the medullar. The medullar looks like a tulip bulb. Therefore, these are often, in a sign of medical profession insanity, referred to as bulbar signs.
What is the role of EEG, LP and MRI head in the assessment if subacute psychosis if autoimmune encephalitis is suspected?
EEG is usually normal in inorganic psychosis. LP is vital for excluding infectious encephalitis - particularly HSV encephalitis that can be treated with acyclovir. MRI head is normal in 70% of autoimmune encephalitis, but can be helpful in excluding other causes.
What intracytoplasmic protein clusters are present in the neurons of patients with Parkinson disease?
Alpha syneuclein
What are the 3 cardinal symptoms of Parkinsons disease?
Bradykinesia, tremor, and rigidity. A fourth ifbit were to be added would be postural instability
Clinically, what are features that differentiate vascular (infarct related) parkinsons disease from idiopathic parkinsons disease?
Vascular PD classically has more negative symtpoms than positive symptoms. That is bradykinesia and rigidity, without tremor.
What classes of drugs are possible causes of drug induced parkinsons disease?
Anything that inhibits dopamine receptors may be a culprit. This includes metoclopramide and other antiemetics, antipsychotics, some opiate-like drugs.
Multiple system atrophy is a Parkinsons Plus syndrome. What are its two subtypes and their classical clinical features?
MSA-P (for parkinsonian) is the first subtype. It features symmetric parkinsonism at the onset. MSA-C (for cerebellar) is the second subtype. It features cerebellar atrophy with cerebellar syndrome. BOTH feature early and prominent autonomic dysfunction- impotence, orthostatic hypotension, constipation, urinary frequency.
Which medication is least likely to worsen parkinson features of Lewy body dementia whilst treating its psychiatric symptoms?
Clozapine is hands down the best, but quetiapine is often more practical.
What are the intracytoplasmic inclusions seen in the neurons of patients with Lewy Body Dementia?
alpha-syneuclein (also known as Lewy bodies!)
What medications are used in Lewy body dementia?
Although the parkinsonian and psychiatric symtpoms of Lewy Body Dementia are dopaminergic in nature, they classically don’t respond well to dopamine replacement therapy or therapies that increase synaptic dopamine concentration, and these medications usually worsen the patients cognitive impairment or psychiatric features. Instead antipsychotic medications (clozapine or quetiapine) and cholinesterase inhibitors (like donezapil) are used as LBD pts also develop a loss of cholinergic neurons as in seen in Alzheimers disease.
Corticobasal degeneration is a neurodegenerative disease of the Parkinsons Plus group. What are its clinical features?
It has marked usually unilateral parkinsonism and prominent apraxias. The classical feature that distinguishes CBD from PD is alien limb phenomenon- the pt believes that their limb has a mind of its own.
Progressive supranuclear palsy is a neurodegenerative disease of the Parkinsons Plus group. What are its clinical features?
Patients with PSP classically present with parkinsonism and impaired voluntary vertical gaze (supranuclear opthalmoplegia). Impaired downward gaze is the most specific clinical feature. Importantly, infranuclear (brainstem) pathways remain in tact and so dollshead vertical gaze is preserved. Typically, patients present with falls due to vision issues.
What are the Parkinson Plus syndromes?
Multiple system atrophy (symmetric parkinsonism, MSA-p/c, profound autonomic dysfunction), corticobasal degeneration (unilateral parkinsonism, alien limb), Lewy Body Dementia, Progressive supranuclear palsy (voluntary vertical gaze loss down>up, involuntary vertical gaze - ‘dollseye’ - is preserved).
What sensory symptom is most common in patients with parkinsons disease?
Anosima- in 80-100% of patients.
What symptom of Parkinson disease best correlates with percentage of dopaminergic neurons lost in the substantia nigra?
Bradykinesia. Tremor correlates very poorly.
When considering a diagnosis of Parkinsons disease, what symptoms or signs should be considered a red flag suggestive of a possible alternative diagnosis?
Rapidly progressing dementia (lewy body dementia), rapidly progressive course (more likely a parkinsons plus), suspranuclear gaze palsy (PSP), upper motor neurons signs (stroke), cerebellar symptoms (MSA-c), urinary incontinence (MSA or lewy body dementia), early symptomatic postural hypotension within 5 years (MSA), early falls (MSA or PSP).
What is the point of carbidopa when combined with levodopa?
L-dopa is a form of dopamine that crosses the blood brain barrier and can be taken orally. Normally however, l-dopa would be enzymatically degraded in the gut by aromatic-amino acid decarboxylases. Carbidopa inhibits these enzymes prolonging increasing the amount of L-dopa absorbed. COMT inhibitors such as entacapone can be used with a similar role, as COMT degrades L-dopa peripherally.
What is the role of amantidine in Parkinsons disease?
Aids in the treatment of tremor, but is most helpful in alleviating the symptoms of levodopa induced dyskinesias.
What is the major contraindication for deep brain stimulator insertion in patients with parkinson disease?
Cognitive impairment. Worsening cognitive function was reported with the insertion of deep brain stimulators.
Rasageline and selegiline are a first line treatment option for mild-moderate parkinsons disease in patients under 75. How do they work and what is their concerning side effect?
Monoamine oxidise B inhibitors (MAO-B). They work by impairing the synaptic breakdown of dopamine and other monoamine neutransmitters thus increasing their synaptic concentration and mitigating parkinsonism associated with dopamine deficiency.
Autodomal dominant cerebellar ataxia/spinocerebellar ataxia is genetic disease caused by what type of gene mutation?
CAG repeats of various lengths in SAC genes.
Where is Brocas area?
Frontal lobe of dominent hemisphere.
What are the the features of dominent parietal lobe defects?
Agraphia, acalculia, finger angosia, left/right descrimination failure
What are the features of an internal capsular infarct?
Contralateral face, arm and leg weakness. Upper motor neuron signs including spacticity, hyperreflexia. No cortical signs.
What areas are involved in a dysarthria and clummsy hand syndrome?
Lacunar stroke - can involve internal capsule or anterior part of contralateral pons.
Ataxia hemiparesis is a lacunar syndrome. Where is the infarct?
Corona radiata, pons or internal capsule.
In the brainstem, do the motor tracts travel laterally or medially?
Medially!
Where does the medial longitudinal fasciculous run?
Fromt he pons to the midbrain, medially! Part of medial brainstem stroke syndromes causing INOs.
What’s a good way of remembering which cranial nerves are lateral, and which nerves are medial?
If the cranial nerve number divides into twelve, then its medial. If it doesn’t, it’s lateral.
What classically leads to a homonymous hemianopia with macular sparing?
Occipatal infarct from a P1 branch cva
Where do the motor fibres decussate in the brainstem?
The medullar
If you have a medullary syndrome with a horners on the right, what does this tell you?
It tells you the lesion is on the right. If given a question that is clearly a lateral medullary syndrome with a horner’s syndrome, then use the side of the horner’s to tell you the side of the lesion.
What is a key difference between a conus medullaris and cauda equine?
Conus medullaris is a central upper motor neuron phenomenon. More defined areas of sensation loss. Erectile dysfunction is a feature. Minimal pain - but critically - Up going plantars!
What does C5 do at each joint?
Abducts shoulders, flexes elbow, allows supination of forearm.
What does C6 do with regards to joint movement?
Elbow extension AND flexion, and wrist extension.
C7 does what with regards to joint movements?
Moves the wrist and extends the elbow.
What does C8 do over the joints?
Flexes and extends the fingers.
Where is the dermatome for C7?
Middle finger
What nerve roots are involved in the triceps reflex?
C7/8
What is the classic feature of an axillary nerve palsy?
Deltoid weakness and patch of numbness over the shoulder
What determines the amount of clawing seen in an ulnar claw?
How distal the lesion is. More distal, more clawing.
Whatas the differnece beteween a femoral nerve and an L2 nerve problem?
Knee movement is preserved in L2 issues. Femoral nerve impairs hip and knee, L2 just imparis the hip.
What roots are involved in each trunk of the brachial plexus?
C5-6 (upper trunk), C7 (middle trunk), C8/T1 (lower trunk)
What innervates the lateral thigh, and what innervates the medial thigh?
Lateral cutaneous nerve of the thigh does lateral, femoral nerve does medial.
How do you differntiate between a femoral nerve palsy and an L3 nerve palsy?
L3 root problem causes issues hip adduction. Femoral nerves do not.
L5 has actions across many joints. However, it has one critical action that helps differentiate it from peripheral nerve problems. What it is?
Dorsiflexion of the great toe.
Which nerve roots control inversion and eversion of the ankle?
Inversion is controlled by L4/5, and everions is L5/S1
If you have a pure sensory syndrome from a thalamic infarct, is it contralateral or ipsilateral to the lesion?
Contralateral
Do cranial nerves decussate to their motor targets?
No, they control ipsilateral facial structures (and ipisilateral SCM and traps for the XI nerve)
Why do patients get CNVII nerve symptoms when there is medial pons disease?
Becuase the fibres come to VIIth nerve nucleus in the lateral pons from cortical structures higher up by wrapping first medially around the 6th nerve nucleus.
What nerve injury causes isolated elbow extension weakness?
Musculocutaneous nerve.
What innervates the triceps?
The radial nerve. Yes, it starts that far up.
What movements are done by the common peroneal nerve?>
Dorsiflexion and eversion. Remember an L5 lesion does inversion and eversion.
What does the tibial nerve do with regards to foot movements?
It does plantar flexion and ankle inversion - the opposite of common peroneal nerve.
Neuromyelitis optica syndrome often presents with optic neuritis. What else does it present with?
Hiccups and vomiting is common.
Ethambutol causes an optic neuropathy. What are its features?
Colour vision loss. Not normally painful.
What is the classic eye finding on the retina in neurosyphillis? (and other retinal infections)
Retinal star
What is the core criteria for the diagnosis of Idiopathic Parkinson’s disease?
Bradykinesia must be present. Only one of rigidity OR tremor must be present to make the diagnosis.
Small amplitude, rapid (10Hz) worse on movement, head and torso involvement tremors are most compatible with what type of tremor?
Essential tremor
What is a Holms tremor?
Progressive. Classically very large amplitude and slow (3Hz). Happens all the time - at rest, with movement. Clasically is a pronation/supination movement. Often associated with previous brain injury affecting the red nucleus - stroke or MS are classic.
Dystonic tremors. What are they?
A function of pulling the head (usually the SCM isvolved) away from an inappropriately contracting SCM. Can occur in other muscles, but a classic no-no tremor.
Cerebellar tremor. What does it look like?
Fine tremor initially, but when reaching out to grab something, the tremour gets large amplitude. It’s slow normally - 2hz. The disease is progressive.
What are you likely to find in MGUS IgM related neuropathy?
Distal demyelinating sensory neuropathy. So, on NCS you would see reduced latencies.
Is multifocal motor neuropathy an axonal degeneration of demyelinating problem?
It’s a demyelinating problem. Classically see like a foot drop and wrist drop or some other mix of these things. Classically not painful, and comes on slower than mononeuritis multiplex.
During compression neuropathy, how do symptoms and nerve conduction studies evolve?
Initially, compression causes demyelination involving the sensory nerves. Then, it starts to lead to axonal degeneration. Then eventually the motor nerves become involved.
Miller fischer syndrome is what triad?
Opthalmaplegia, ataxia and areflexia. It’s a subtype of AIDP.
When does AIDP become CIDP?
After 8 weeks.
Why are nerve conduction studies normal in sensory radiculopathies?
Because the compression of the nerve occurs prior to the dorsal root nerve ganglion (before the periperal sensory nerve bodies). The NCS loop is able to occur unimpeded.
What’s the classic difference between lambert eaton syndrome and myaesthenia gravis?
Myaesthenia gravis is fatiguable. LES gets better with exercise!
What is the pathognomonic feature of LGI1 autoimmune encephalitis?
Facio-brachial dystonic seizures.
What cancer is anti-hu classically associated with?
Small cell lung cancer
What is the most common infective cause of a rhomboencephalitis (brainstem involvement)?
Listeria
Waht are the featuers of paroxysmal hemicrania?
Classically invovles a branch of CNV. Lasts 5-10mins. Happens multiple times per day.
What is the significance of a negative head-impulse test?
The head impulse test is positive when the eyes saccade back to the nose when the head is wobbled side to side. This indicates an issue in the reflex arc involving the peripheral nerves. This a reasurring sign in someone with vertigo and nystagmus. If they have a normal occulovestibular reflex (are able to keep focus when their head is wobbling), this is concerning for a stroke.
Superior Canall Dehiscence is classically asscociated with what symptom?
Tinitis and audible verticle nystagmus triggered by loud noises.
What is the classic inflammatory disease that needs looking for when bilateral facial nerve palsy is seen?
Sarcoidosis
What is the cytochrome P450 enzyme utilised by clopidogrel to be converted from its pro-drug to active drug form?
CYP2C19
What platelet count is an absolute contraindication to tpa?
Less than 80
How long does it take DWI to become positive in a stroke?
5 mins
Which tPA agent has the greatest benefit prior to ECR?
Tenecteplase is better than alteplase
When does T2 Flare MR imaging become positive in stroke?
4.5hrs. This is interesting - it means if you have a wake up stroke, do a T2 flare and its negative, but then the DWI is positive for stroke, you can do say that the stroke was likely within the last 4.5hrs and give tPA
When is it safe to given tPA up to if the CTP shows good penumbra?
9hrs
Hemicraniectomy is indicated in what ICH scenario?
Any age with >50% of MCA territory involved.
What do the Australian stroke guidelines say is the maximum systolic blood pressure that should be achieved after the acute phase of an ischaemic stroke is over?
Lass than 130mm/Hg
Which CYP enzyme is associated with clopidogrel resistance?
CYP219 mutations that don’t allow pro-drug to drug conversion.
CEA is considered in men with symptomatic carotid occlusions of what percentage stenosis?
> 50%
CEA is considered in men with asymptomatic carotid occlusions of what percentage stenosis?
> 70%
What is the treatment for carotid artery dissection?
Aspirin alone.
What is the reversal agent for dabigatran?
Idaracizumab
What is the indication for PFO closure in stroke patients?
Age <60 without any other cause found. Take no notice of shunt size or DVT history.
What is the blood pressure target in ICH?
140mmHg systolic
What are the possible sequelae of cerebral amyloid angiopathy?
Convexity SAH, lobar haemorrhages, white matter disease and cortical infarcts, inflammatory disease and vasculitis, cortical microhaemorrhages, cortical superficial siderosis, dementia.
What is the treatment for VITT related venous sinus thrombosis?
Bilivirudin + IVIG + steroids
Which HLA gene is associated with MS?
HLA-DRB115
Which virus is associated with increased risk of MS?
EBV
What lesion location does not contribute to the distribution in space criteria for MS?
The optic nerve
Which immunosuprresing drugs cause hair loss?
Teriflunamide and leflunamide
What MS drug causes first dose macular oedema and bradycardia?
Fingolimod
Do you need an oral taper with an acute MS relapse?
Nope. You just give 3 days of 1g IV methylpred then stop. Can even use 1mg/kg oral.
What drug is contraindicated in pts with CYP2C9 gene mutations?
Siponimod
What MS drug can cause ITP, graves disease and Goodpastures syndrome?
Alemtuzumab
What is the target of alemtuzumab?
CD52
What does satralizumab target?
IL-6 receptor recycling initiator
What does inebilizumab target?
Targets CD19
Whats the difference between ocrelizumab and ofatumumab?
Both target CD20 on B cells, however ofatumumab is subcut and ocrelizumab is IV
What is the drug of choice for secondary progressive MS? Based on trial data.
The best drug at the moment is siponimod. Lancet study showed secondary progressive MS slowing with siponimod.
What is the drug of choice for primary progressive MS?
Ocrelizumab is the only drug good evidence for it.
What is the first line treatment for essential tremor?
Propanolol
First line treatment for REM sleep disturbance?
Clonazapam`
Main side effects starting L-Dopa?
Nausea vomiting and orthostatic hypotension
What parkinsons drug is most likely to cause delirium?
Amantidine
Tyramine hypertensive crisis is caused by what?
Accumulation of pre-amine neurtransmitters (particularly adrenaline) - caused by giving too much MAO inhibitors for parkinsons disease
Pimavanserin is used for what?
Managing the hallucinations seen in Parkinson’s disease.
What is the relevant mutation in FXTAS?
Trinucleotide repeat gene in the FXTAS gene.
Most sensitive test for Listeria encephalitis is what?
Blood cultures. Very hard to get out of the CSF,.
What is the test of choice for diagnosing Japanese Viral encephalitis?
It’s
In autoimmune encepahlitis, what part of the neuron is targeted - intracellular or extracellular epitopes?
Extracellular. Contrast with paraneoplastic syndromes associated with abs targeting intracellular epitopes.
What are the cancers most commonly associated with?
Thymoma, breast cancer, teratoma, small cell breast cancer
Vibration and proprioception use what fibres?
Large alpha and beta fibres
POEMs is the result of elevation of what blood marker?
VEGF in plasma
Anti-MAG and MGUS central and peripheral are the result of what immunoglobulin paraprotein? (Ig subclass?)
IgM
What’s the best treatment for small fibre neuropathy?
Amitryptaline, then duloxetine
What is the ab associated with Miller -Fischer syndrome?
Anti-GQ1b
What is the order of changes seen on NCS for AIDP?
F wave issues, then motor demyelinating changes, then sensory demyelinating issues.
What is the antibody found in multifocal motor neuropathy?
Anti-GM1
Myaesthenic gravis is a problem due to binding to which part of the synapse?
Post-synaptic. Can be associated with the anti-MUSK ab.
Lambert-eaton syndrome is a problem with antibodies binding to what part for the neuromuscular junction?
Pre-synaptic binding issue.
What is efgatigimod?
Fc-neonatal receptor blocker. The normal function of this receptor is recycling IgG and extending its half life. So, by blocking this, you are reducing the concentration of pathogenic IgG in in myesthenia gravis.
Which immunosuppression is safe in pregenancy?
Azathioprine
What is the target of pathogenic abs in Lambert Eaton syndrome?
VGCC
What is the drug treatment for lambert Eaton syndrome?
3-4 Diaminopyridine
What HLA predisposes to lambert eaton syndrome?
What is patisiran for?
Patisiran is an RNA infterference therapeutic agent. In 2018, it was shown to be an effective agent in the treatment of the rare hereditary transthyretin amyloidosis. This drug specifically inhibits the liver synthesis of tranthyretin.
Where is calcitonin gene related peptide produced?
Trigeminal ganglion
What is the pathophysiology of superior canal dehiscence?
Thinning fo the bone overlying the semicircular canal
What drug is an agonist 5HTB&D receptors?
Sumitriptan. There is another one called lasmiditan that just blocks the 5HTF one that
Which gene is implicated in familial hemiplegic migraine?
CACAN1A
Which drug is used to treat hemicrania continua as a trial?
Indomethacin
What is first line for cluster headache prophylaxis?>
Verapamil
What is the first line treatement for SUNCT/SUNA headaches?
Lamotrigene
What does galcanezumab target with regard to migraine?
Calcitonin gene related peptide.
What is trigeminal neuralgia usually caused by?
Most trigeminal neuralgia is caused by demyelination of the nerve root entry zone due to superior cerebellar artery impingement.
In young women with new generalised epilepsy, what do you give?
Lamotrigine
What epilepsy drug causes hyperaemia and acute liver failure in some patients?
Sodium valproate
Which epilepsy drug is a an autoinducer of CYP3A4?
Carbemazipine
Which drug cases termor and ataxia after many years of use due to a mitochondialopathies?
Sodium valproate. This is actually why you don’t use it in young children with a seziure, as they may have an underlying mitochondrial disease.
Which anti-convulsant can cause psychosis and irritability?
Levetriactam
Which antiepileptic potentiates carbamazepine?
Phenytoin
Which anti-epileptic do you need to slowly uptitrate?
Lacosamide
What are second line for status epilepticus?
Phenytoin, levetiracetam, phenobarbital, sodium valproate
During pregnancy, what antiepileptics can be used?
Lamotrigine, carbemazipine, gabpentin, levetriazetam
What is first line treatment for status epilepticus?
Benzodiazepine
What are the side effects of phenytoin?
Hirsutism, gingival hyperplasia, and some neuropathies.
The urticle and saccule are responsible for regulating what movement of the head?
Linear movements
What nerve is most susceptible to damage with a fracture of the humerus?
The radial nerve.
