Systemic Neurology 2

Mah Belly Beans

100

Hypernatremia over this number is most commonly associated with neurologic symptoms/deterioration

> 160 

200

As a general rule of thumb: Neurologic symptoms begin with sodium less than this number mmol/L or a rapid change of this number from any baseline 

< 125; Change of 20 rapidly 

300

A patient presents with altered mental status rapidly over 24 hours while in the hospital. They had initially described muscle spasms of the hands and feet and even noticed flexion of his fingers during BP checks. You were consulted due to a GTC. What lab abnormality is likely present

hypocalcemia -- seizures usually present when < 2; neuromuscular symptoms often when < 3

Trousseau sign can occur with hypomagnesemia, but usually due to concomitant hypocalcemia 

400

A dialysis patient present to yours clinic after recently starting their first couple of sessions of dialysis. They noted that they have had wrist drop since that time that has not improved and they had complained of some pain. Your exam reveals weakness of wrist extension and arm extension. Sensory loss along posterior arm and forearm is also noted. Pulses are normal in the affected arm and no skin changes are noted. What is the diagnosis? 

Ischemic monomelic neuropathy -- secondary to dialysis catheter placement -- blood can be shunted away from the nerve causing a mononeuropathy. 

500

This epileptiform EEG finding can be found in patient with chronic renal failure

bilateral spike and wave abnormalities -- which usually have no clinical significance on its own and are often asymptomatic 

My liver hurts, acutely

100

This is the criteria used to assess degree of hepatic encephalopathy

West Haven Critereia

25% of Grade 3 and 75% of Grade 4 have cerebral edema -- CT scan 

200

True/False acute hepatic encephalopathy/hyperammonemia directly causes anisocoria/pupillary changes due to optic nerve/sympathetic dysfunction

False: Pupillary signs are concerning signs of herniation that are secondary from cerebral edema

300

Up to this percent (to the nearest 5%) of patients with acute hepatic encephalopathy have subclinical seizures

33%

400

These findings on exam/labs/vitals are indicative of risk of cerebral edema from liver failure

1. Sepsis/SIRS

2. High grade encephalopathy (clinically)

3. Ammonia > 100

4. Renal failure

500

These 2 anti-seizure medications are recommended for seizures secondary to liver failure; 

Bonus: name 3 that should NOT be used

1. Levetiracetam, Lacosamide

2. Phenytoin, Valproate, carbamazepine

My liver hurts, chronically

100

This percent of patients with cirrhosis have covert hepatic encephalopathy (to the nearest 10%)

85%

200

These are the symptoms of covert hepatic encephalopathy

apraxia, sleep-wake inversion, and personality changes; can use the animal naming test to stratify treatment of ammonia (15 animals in 60 seconds)

300

These 3 medications commonly cause worsening hepatic encephalopathy

1. Opiates

2. Benzodiazepines

3. PPI

400

Describe the findings and what syndrome associated with chronic liver disease 

1. Symmetric T1 hyperintensities of the globus pallidus - manganese toxicity (due to portosystemic shunting)

2. Acquired hepatocellular degeneration: non-fluctuating presence of tremor, dystonia, oral dyskinesias, parkinsonism, and cerebellar dysfunction

500

This is the treatment of acquired hepatocellular degeneration

Liver transplant -- only small trials demonstrated mild improvement with levodopa or bromocriptine 

Im so hormonal

100

Describe the clinical situation in which prolactin is actually helpful in seizure evaluation

1. Helpful for temporal lobe seizures/GTC seizures vs non-epileptic events

2. Having a baseline prolactin

3. Obtain level within 10-20 minutes of suspected event and > 2 times baseline

Of note, syncope can cause transient hyperprolactinemia. Sensitivity is still 46-60% and low NPV

200

These two syndromes/pattern of vision loss are commonly seen with pituitary macroadenomas

1. Bitemporal hemianopia -- optic chiasm

2. Junctional scotoma with APD (ipsilateral central scotoma with contralateral superior temporal VF deficit) -- junction of optic nerve and optci chiasm

300

Patient who previously had vision changes and had pituitary tumors resected should be monitored by neuro-ophthalmology for color vision/static perimetry due to this % of patients (range of 10%) having subclinical vision loss as first sign of tumor recurrence

5-15%

400

Patient presents after new headache with nausea and vomiting and was admitted yesterday. CT head was negative. You were asked to see her the next day and you note their lab testing shows a low TSH and low T4. Upon evaluation, the headache is not resolved and you note ptosis of the left eye, blurry vision of both eyes, and double vision. What is the most likely diagnosis and what is next step? 

1. Pituitary apoplexy

2. MRI brain with and without pituitary protocol

- CT sensitivity: 21-46%

- MRI sensitivity: 88-90%

500

this condition has a classical presentation of unilateral extremity pain that is often followed by weakness that is often associated GLP-1s and rapid changes in glucose fluctuations. 

Diabetic lumbosacral radiculoplexus neuropathy

Im still hormonal

100

This metabolic abnormality is often associated with a delayed relaxation phase of muscle stretch reflexes (Woltman sign) 

Hypothyroidism

200

Name 3 peripheral neurologic clinical manifestations that are associated with significant hyperthyroidism

1. Myopathy

2. Peripheral neuropathy

3. Thyrotoxic periodic paralysis (sudden periods of weakness after high carb meal or exercise)

300

Patient with new diagnosis of diabetes and treatment comes to your clinic after a few months of burning pain in his legs and feet with orthostasis. 

Treatment-induced neuropathy of diabetes

400

This movement disorder is commonly present with significantly elevated glucose and what imaging findings are present. 

1. Unilateral hemichorea and hemiballism

2. T1 hyperintensity in contralateral striatum

500

65 yo Patient presents with severe unilateral thoracic pain that is worse at night and has progressed over the last few weeks. There is no rash, structural imaging found no evidence of neuroforaminal narrowing or cord changes and it resolved after around 6-12 weeks without treatment. They have a PMHx of HTN, HLD, DM2, CAD, B12 deficiency What is the diagnosis?  

Diabetic thoracic radiculopathy