Intermediate Neurology Flashcards
A 60 year old woman with resting tremor, bradykinesia, postural instability, foot drag, and masked facies is diagnosed with neuronal loss in the substantia nigra and is presenting for total knee replacement. She is on the normal assortment of medications for her above medical condition including levodopa/ carbidopa, bromocriptine, and selegiline. She reports she also has hypertension, post-operative nausea and vomiting and acid reflux. Which of the following medications would be MOST appropriate in her perioperative course:
A. Ephedrine for hypotension B. Meperidine for post-operative pain C. Propofol for induction D. Metoclopramide for premedication E. Droperidol for post-operative vom
Explain each one
C: Propofol for induction
The above patient has Parkinson’s disease, characterized by the above symptoms and loss of dopamine producing neurons in the substantia nigra. Patients on long-term levodopa often have problems with haemodynamic stability due to catecholamine depletion, autonomic instability, and catecholamine sensitization making direct acting vasopressors such as phenylephrine and epinephrine preferred over indirect ones such as ephedrine. Induction for patients with Parkinsosn’s disease should be done carefully as autonomic instability can lead to significant swings in blood pressure and reduced or slowly administered doses of propofol can accomplish this goal. Mepreridine is contraindicated in the setting of MAOIs such as selegiline as haemodynamic instability, hyperpyrexia, and coma can result. Dopamine antagonists such as metoclopramide and droperidol can significantly exacerbate parkinsonian symptoms.
Can you reverse remifentanil with naloxone?
Yes!
Generalized vs complex seizure. What do generalized seizures include?
This patient’s eye blinking can be either a partial seizure or tic disorder, but the infrequency of the symptoms as well as the association with tinnitus makes tic disorder very unlikely. The seizure progresses from an awake responsive state to one with impaired consciousness making the partial seizure “complex.” Generalized seizures characteristically have no ‘local’ onset, have impaired consciousness throughout and include absence as well as tonic/ clonic/ tonic-clonic/ atonic seizures. It is important to know what seizure symptoms patients’ have as it is not uncommon to occur post-operatively.
A 50 year old man with traumatic brain injury (TBI) is started on levitiracetam (Keppra) immediately after the injury. The intern asks you how long it should be continued and you respond:
For severe head injury, it should be continued for 7 days Antiseizure medications (most studied is perhaps phenytoin) show significant reductions in early seizures following TBI. Early seizures are defined as the first 7 days, whereas later seizures are after 7 days. The incidence of seizures increases significantly with the severity of TBI and is highest with penetrating missile injuries. It is questionable if the benefits outweigh the risks in more mild TBI. Antiseizure medications appear to be ineffective in preventing late seizures. Late seizures, especially those occurring more than a month after the TBI tend to be associated with an eliptogenic process, whereas early seizures are often isolated and do not predispose patients to late seizures.
Status eoilepticus-why is it so dangerous? Who does it mostly happen to? Time to permanent neurological injury?
Persistent sustained seizures can lead to neuronal injury via supply demand mismatches (increased O2 demand without increased O2 delivery) just like any other stressed organ. Permanent neurologic injury can result within 5 minutes. Myotonic jerks is an especially poor prognostic sign, although not very specific. Although the musculoskeletal injuries associated with tonic/ clonic seizures such as bone fracture, rhabdomyolysis, and ligament injuries are worrisome, it is the neuronal injury which makes status epilepticus an emergency. Most cases of status epilepticus (~ 75%) are not in patients with previous seizure disorders, but instead significant medical/ surgical conditions such as anoxia, cerebral haemorrhage, stroke, metabolic derangements, and alcoholic withdrawal.
In a seizure, priority number one-
AIRWAY!!!
Why would you not use ketamine in a patient with a history of seizures?
Ketamine is not a good first line therapy for seizures as seizures can be precipitated by its use in certain individuals with underlying epilepsy.
Which 3 anesthetic drugs can decrease the seizure threshold?
Etomidate, ketamine, and methohexital all can decrease the seizure threshold,
Following multiple large doses of meperidine, a patient has a seizure. Which of the following medical conditions is most likely true regarding this patient:
A. Coronary artery disease (CAD)
B. Chronic renal insufficiency (CRI/ CKD)
C. Chronic obstructive pulmonary disease (COPD)
D. Anterior spinal cord syndrome
B: Chronic renal insufficiency (CRI/ CKD)
Normeperidine, a metabolite of meperidine can accumulate in the setting of kidney failure and lead to seizures.
What is true regarding an asymptomatic carotid bruit found on physical exam:
A. The patient is at increased risk of concomitant coronary artery disease (CAD)
B. The patient most likely has aortic stenosis
C. The patient is at increased risk of perioperative stroke
D. At least 70% stenosis is needed to auscultate a cervical bruit
E. More times than not, carotid massage will result in a stroke or TIA
Explain each answer!!!!
A: The patient is at increased risk of concomitant coronary artery disease (CAD)
Carotid bruits are associated with underlying CAD, as the same calcification process happening in the carotid artery often occurs systemically. An asymptomatic bruit; however, does not increase the incidence of perioperative stroke. A late peaking systolic murmur with bilateral bruits is characteristic of aortic stenosis, not an isolated unilateral bruit. A bruit does not necessarily correlate with the amount of stenosis, but at 70% one often may hear a bruit. Carotid massage in the setting of carotid stenosis is a theoretical concern for embolization of plaque, but is not clinically common at all.
How would posterior symptoms, (cerebellar function) present? Which arteries supply this area?
posterior” symptoms which may include cerebellar functions (coordination, balance, etc), occipital (bilateral visual) as well as more generalized symptoms such as weakness, amnesia, and confusion. The posterior portion of the circle of Willis is supplied by the basilar artery and the cerebellum is primarily supplied by arteries off the vertebral and basilar arteries
The most common cause of intraoperative stroke from CEA is from
Embolism
A 60 year old man with stroke 6 months ago has no residual symptoms although he had mild hand weakness and abnormal sensations for 2 weeks following the stroke. He presents with bowel obstruction and receives succinylcholine on induction. What is the most likely response to succinylcholine in this patient:
A. Hyperkalaemic cardiac arrest B. Increase in serum potassium by 0.5 mEq/ L C. Malignant hyperthermia D. Masseter muscle rigidity (MMR) E. Prolonged paralysis
B: Increase in serum potassium by 0.5 mEq/ L
Denervation injuries including stroke is a risk factor for upregulation of extrajunctional acetylcholine (Ach) receptors outside the muscle endplate. Depolarization of large quanities of these extrajunctional receptors can result in hyperkalaemia and even cardiac arrest. In the setting of ‘mild’ stroke where there is no persistent motor deficit, significant extrajunctional upregulation of receptors is very unlikely, therefore making the risk of hyperkalaemia very unlikely. In normal patients, the depolarization of multitudes of junctional Ach receptors raises potassium serum levels by 0.5 to 1.0 mEq/L transiently.
Cerebral palsy and succinylcholine?
Cerebral palsy is not a risk factor for hyperkalaemia even in the setting of contractures as extrajunctional acetylcholine receptors are not upregulated. A prefasciculation dose, in all patients, may decrease myalgia following succinylcholine administration. Cereberal palsy is not a risk factor for malignant hyperthermia and these patients are put on dantrolene to treat spasticity.
Which of the following pediatric patients would latex allergy be most likely to occur in:
A. Craniostenosis
B. Myelomeningocele
C. Cerebral palsy
The correct answer is: B: Myelomeningocele
Latex allergies occur most often in children with myelomeningocele, spina bifida, genitourinary disease, indwelling tubes, and multiple surgeries (as a child). Latex allergies often coexist with banana, avocado, and kiwi allergies, among others.
Is epidural okay for people with MS?
Epidural anesthesia is generally considered safe,
In MS is sux contraindicated?
Succinylcholine is relatively contraindicated in MS, with a stronger (maybe even absolute) contraindication in the setting of paresis and paralysis as it is a upper motor neuron demyelination causing this.
Hyperthermia vs hypothermia-which one makes MS worse?
Hyperthermia, not hypothermia exacerbates MS, and this is a classic boards topic.
Which of the following neurological and neuromuscular disorders is succinylcholine NOT contraindicated in:
A. Duchenne’s muscular dystrophy (DMD) B. Guillain-Barre syndrome (GBS) C. Myasthenia Gravis (MG) D. Myotonic dystrophy (MyoD) E. Amyotrophic Lateral Sclerosis (ALS)
Myasthenia Gravis (MG)
A partner is in the process of placing a spinal anesthetic in a patient with Guillian-Barre syndrome (GBS) as you come to take the case over from her. A 22 g spinal needle is placed between L3 and L4 with CSF dripping back. What would you tell your partner at this time:
A. The patient is now at increased risk of having a GBS exacerbation
B. If the local anesthetic is not injected, the patient will not be at increased risk of having a GBS exacerbation
C. There is no contraindication to spinal anesthetic in GBS patients
D. There is no contraindication to spinal anesthetic in GBS patients so long as isobaric local anesthetic is used
E. There is no contraindication to spinal anesthetic in GBS patients so long as hyperbaric local anesthetic is used
B: If the local anesthetic is not injected, the patient will not be at increased risk of having a GBS exacerbation
This is a hard question, as you have to know exactly what is and what is not safe in GBS. The clue to answering this is the knowledge that spinal (and epidural) anesthetics are considered contraindicated (like MS as discussed in question 19, the evidence is sparse and weak) and lumbar punctures (LPs) are performed in GBS patients routinely by neurologists without sequelae. The anesthesiologist has placed a spinal needle in the patient which is equivalent to an LP, but until the anesthetic is injected, it would not be expected to exacerbate symptoms. There is not enough data to determine if the baricity of the anesthetic has any bearing on exacerbating the symptoms.
What are four big perioperative concerns for patients with MyoD? And does hyper or hypo hurt them? Regarding contra tires-what 3 things to avoid?
There are four big perioperative concerns with patients with MyoD for anesthesiologists 1) contractures; 2) sensitivity to anesthetics; 3) aspiration risk; and 4) theoretical increased risk of malignant hyperthermia (which is probably FALSE!). Regarding contractures, three big things to avoid: 1) succinylcholine (see question 21 – sustained contractures); 2) reversal of muscle relaxation with anticholinesterases (sustained contractures); and 3) hypothermia leading to shivering and then contractures. Contractures can be so severe, ventilation and intubation is impossible.
Myasthenia Gravis-what is it? Which neuromuscular blockers are they sensitive to? Any relation to thymus issues?
C: Patients with MG are exquisitely sensitive to nondepolarizing muscle relaxants
MG is characterized by Abs to Ach-Rs at the neuromuscular junctions on skeletal muscle and does not affect smooth muscle. Because there are so few receptors to block in MG, nondepolarizing muscle relaxants can cause profound paralysis at very low doses while supranormal amounts of depolarizing relaxants are needed. There is a theoretical increased risk of phase II block with these patients after using succinylcholine due to the increased dose and use of acetylcholinesterase inhibitors (for MG symptoms) which decrease succinycholine’s metabolism (board classic). Most patients with MG have laboratory evidence of Ach-R Abs and thymus hyperplasia or thymomas. MG has four different subtypes with type I being the most mild and limited at extraocular muscles. Other types (IIA, IIB, III, IV) have progressively more symptoms affecting respiratory and bulbar muscle groups putting them at increased risk for respiratory failure, airway obstruction, and aspiratio
A 45 year old woman with myasthenia gravis (MG) presents for trigger finger release and complains of increasing weakness, especially today. Her normal dose of pyridostigmine 60 mg four times daily was increased to 80 mg two days ago by her doctor. She reports having taken her prescribed dose three hours ago this morning. What is the best way to elucidate the cause of this patient’s weakness:
A. 5 mg edrophonim IV now and observe
B. 1 mg of glycopyrrolate IV now and observe
C. 1 mg of glycopyrolate now and send to the ED
D. Acetylcholine receptor antibody (Ach-R Ab) titer
E. Urgent plasmapheresis prior to surgery
A: 5 mg edrophonim IV now and observe
Most likely this patient either has rapidly worsening symptoms of MG or a cholinergic crisis. Based on the history both are possible, as increasing doses of pyridostigmine is needed for worsening symptoms, while an overdose of pyridostigmine (dose was just increased two days prior) could cause cholinergic crisis. The ‘tensilon test’ is used to differentiate the two. Edrophonium is given IV, improvement in strength indicates MG causes while increased weakness indicates cholinergic crisis. Other symptoms of cholinergic overdose (salivation, bradycardia, myosis) would be present either way. Atropine would be the ‘antidote,’ in a cholinergic crisis (without MG), and glycopyrolate could also be useful for non central nervous system manifestations. Ach-R Ab titer would take to long for a result, and is also more useful for diagnosis than management. Plasmapheresis can remove circulating Ach-R Ab, but is not common prior to minor surgery.
MG risk of post-operative mechanical ventilation:
disease duration > 6 years, vital capacity < 2.9 L, pyridostigmine > 750 mg / day, or concomitant respiratory disease (not kidney