I feel like maybe I’m getting smarter or something. Or something.

Anyway, here is a list of more stuff learned in neuro:

1) “Frontal release signs” are primitive reflexes, which are signs of disorders that affect the frontal lobes. Examples are the palmar grasp reflex, the rooting reflex, the sucking reflex, and the snout reflex. These reflexes are normally inhibited by frontal lobe activity in the brain, but can be “released” from inhibition if the frontal lobes are damaged.

2) With Broca’s aphasia (comprehension is intact but fluency is affected), you can also find motor impairments. However, if it is the result of an embolism, you won’t have motor findings.

3) With Wernicke’s aphasia (fluency is intact but comprehension is affected) you will never have motor impairments.

4) The inferior branch of the middle cerebral artery is more straight, and hence it’s more likely to be affected by an embolic stroke than the superior branch.

5) Pseudobulbar palsy is a disconnect between the cortical bulbar fibers and the cranial nerves. You can see this with a pure embolic stroke.

6) Only give heparin to a stroke patient if you know there is thrombosis.

7) A “neural intubation” is what you would do for a stroke patient. You would give them mannitol and hyperventilate the patient.

8 ) A stroke causes intracellular edema, so there is no role for steroids. However, a brain tumor causes interstitial edema, so giving steroids can be helpful.

9) A stroke patient should be prescribed a pureed diet (unless otherwise indicated) because the first step involved in swallowing is what is affected by strokes, and not the other steps. This means they can handle pureed food, but not solids or liquids.

10) Transient global amnesia is an anxiety-producing temporary loss of the ability to form new long-term memories that by definition resolves within 24 hours and most commonly affects the middle-aged or elderly.

11) Jacksonian March involves the progression of a seizure, and can be seen as starting in the eyelids, and progressively moving down the body. (I witnessed one.)

12) How to differentiate between a real seizure and a pseudoseizure. With a real seizure, during the post-ictal state you will see a positive Babinski sign, dilated pupils, and elevated prolactin levels.

13) During a seizure, you should expect the gaze preference to be towards the seizing side.

14) The treatment for status epilepticus is benzodiazepines, intubation, and a dilantin drip. If that doesn’t work, you can try phenobarbitol.

15) Never give a muscle relaxant to a patient having a seizure.

16) Electrographic seizures are evidence of a seizure on EEG, but with no clinical manifestations.

17) With nystagmus, the fast component is towards the affected side (and I finally got to see it in real life).

18) The frontal gaze center affects the opposite side (left controls right), and with the pontine center, it is the same side (left controls left).

19) What internuclear opthalmoplegia is (a disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction), and what can cause it (multiple sclerosis, TB, fungal infections, small vessel lacunar strokes.)

20) Flu vaccinations can cause Acute disseminated encephalomyelitis (ADEM). Scary!

21) If you see bilateral Periodic lateralizing epileptiform discharge (PLED), it’s almost certainly being caused by herpes encephalitis.

22) You must be careful with correcting hyponatremia, because if you do it too quickly, you can cause central pontine myelinosis.

23) With multiple sclerosis, the plaque formations can cause seizures (same with Alzheimer’s disease.)

Now you can see the fun I’m having!

Note: Photos are me and one of my fave books, Robbins & Cotran Pathologic Basis of Disease, Seventh Edition

Today was a good day in neuro. Our patient presented with signs of a CVA (cerebrovascular accident), and we were able to deduce that the likely culprit was an ischemic infarct of the MCA (middle cerebral artery).

Also, I learned some stuff:

1) The differential diagnosis of ptosis.
a) muscular (myasthenia gravis, muscular dystrophy, progressive external opthalmoplegia)
b) third nerve palsy (tumor, or vasovasorum (diabetes mellitus)
c) metabolic
d) traumatic (cataract surgery)

2) If you see unilateral ptosis w/ normal pupil size, it’s likely due to diabetes mellitus. If you see unilateral ptosis w/ a dilated pupil, it’s a third nerve palsy

3) The most common cause of bilateral third nerve palsy is a CVA (number one type of CVA is of PCA (posterior communicating artery).

4) If you need to do carotid surgery on an elderly patient, or one with multiple comorbidities, it’s better to place a stent, rather than doing an endarterectomy.

5) If you have a pontine CVA, the gaze preference will be to the SAME side as the weakness.

6) If you have an MCA CVA, the gaze preference will be to the OPPOSITE side of the weakness (as we saw with our patient).

7) If you have increased intracranial pressure, your body will compensate by becoming hypertensive and bradycardic. You may also see hyperventilation (this can be utilized as a treatment as well).

More fun to come!

Note: Since my last photos were so popular, I took some more to go along with this post. The book is Bates’ Guide to Physical Examination and History Taking, from the chapter on neurological examinations.

Okay, for the record, getting up at 5 a.m. every day and walking in the pitch black darkness to the hospital is becoming very old. I am NOT a morning person, and this is killing me! But I really shouldn’t be complaining, since I am home (and sometimes back in bed) by 8:30 a.m.

Anyway, since I promised, and since it made me feel better the last time I did it, here are some more “stuff learned” items from my neurology rotation:

1) All about myasthenia gravis, including diagnosis and treatment. (It’s an autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatiguability.)

2) When/how/and why not to do the tensilon challenge test to diagnose myasthenia gravis. (Do it in the ICU, or somewhere where you have a crash cart ready.)

3) The differential diagnosis of generalized weakness, including Addison’s disease, hyper and hypokalemia, parathyroid disturbances, hypothyroidism, and myasthenia gravis.

4) What external progressive ophthalmoplegia is. (Causes weakness of external eye muscles.)

5) The difference between a thymoma (anti-thymus AB +) and thymus hyperplasia (anti-thymus AB -). You can differentiate the two via MRI.

6) What to do in the case of a myasthenic crisis. (It causes a paralysis of the respiratory muscles. If this happens, you should stop all myasthenia gravis medications. If the vital capacity is less than 500 cc, you must intubate. Then give a large does of steroids or immunoglobulins.)

7) All about normal pressure hydrocephalus, including its presentation (wet, wobbly, and weird), and treatment (possibly place a shunt).

8 ) If a patient walks in with a history of alcohol abuse and lower extremity ataxia only, give them a shot of thiamine.

9) How to diagnose and treat Wernicke-Korsakoff syndrome.

10) A PET scan on an Alzheimer’s patient will likely show decreased activity in the parietal lobe.

11) How to diagnose progressive supranuclear palsy. (It’s a rare degenerative disease involving the gradual deterioration and death of selected areas of the brain.)

12) If you are trying to diagnose normal pressure hydrocephalus, you can do the Mini Mental Status Exam (MMSE) before and after doing a lumbar puncture. If their MMSE score improves, there is a good chance they have normal pressure hydrocephalus.

13) What shunt nephritis is. (It’s rare disease of the kidney that can occur in patients being treated for hydrocephalus with a cerebral shunt.)

Note: I couldn’t find any cool photos to go with this post, so I just snapped a few using Photo Booth of me and my anatomy book. Fun!

I just wrote an blog entry for Medscape, which should be published soon, but the gist is that I’ve been doubting my commitment to medicine recently. Over the past few weeks, I’ve just not been enjoying learning medicine, and I’m thinking that maybe becoming a medical doctor is not what I really want to do. I’ve even been looking into various psychology Ph.D programs over the past few days. I have no idea if this is just a short phase, which will pass, or if it’s the real deal. But I decided to finally admit my doubts to the world. So, there you have it everyone.

I wanted to also get back into the habit of logging my “stuff learned” during my clinical rotations. So, here is a very short list of the things I can recall learning during my neurology rotation so far:

1) What pseudotumor cerebri is, what it looks like on presentation, and how to treat it. Basically, it’s a neurological disorder that is characterized by an increased intracranial pressure (pressure around the brain) in the absence of a tumor or other diseases. Interestingly, it’s still considered idiopathic, although it seems to present in obese women of childbearing age.

2) When performing the Mini Mental Status Exam (MMSE), it’s really important not to skip any items, as you might miss a huge and important finding.

3) What Klippel-Feil Syndrome is, and what it looks like on presentation. I thought this was a particularly interesting case. The syndrome involves fusion of 2 or more of the cervical vertebrae, causing a shortened neck, and a variety of neurological symptoms.

4) What platybasia is, and what it looks like. Platysbasia is a “malformation of the base of the skull due to softening of skull bones or a developmental anomaly, with bulging upwards of the floor of the posterior cranial fossa, upward displacement of the upper cervical vertebrae, and bony impingement on the brainstem.”

That’s it for now. More to come soon in the exciting world of neurology!

Note: Photo was taken days before I left the States to begin medical school.