It had been a very successful series of neurology mobile clinics given the number of patients seen over the last three days, much to the credit of Africanus at Rift Valley Children’s Village, and the partnership we have with Food For His Children that brought patients in to see us at Basodawish. It was now time to resume our neuro clinic at FAME for today and all of next week for tomorrow we would be heading off to the Serengeti for a three-day, two-night adventure. As it was Thursday, though, there would be an educational lecture first, and we had been asked to give today’s talk.
LJ, who just happens to be our new dizziness guru at Penn after six months commuting to Johns Hopkins to work with the world’s expert on this subject, David Zee, agreed to cover this subject for the clinical staff at here at FAME. Though the dizzy patient is perhaps the one most often dreaded by neurologists, LJ thrives in this arena and has found a true niche in which she can not only make a difference for the patients but can also teach others how to properly evaluate these patients. Defining exactly what the patient is complaining of, and its exact nature is absolutely crucial before you can begin to examine the patient and even consider potential etiologies.
One patient who came back to see us today was the gentleman we had previously seen with what appeared to be catatonia, but he was not frankly psychotic, nor did he appear to have schizophrenia as he was too old and functional for that. He had been placed on a benzodiazepine trial (giving a short course of a valium like medication that paradoxically makes the patient more awake and interactive rather than sleepy) to see if he would improve as well as an SSRI antidepressant as that was his most likely underlying psychiatric issue and had led to his catatonia. The family reported that he had responded to the benzo trial by being more interactive and alert, but after the benzos were stopped, he had again developed his psychomotor slowing – they wanted to know whether we could put him back on the benzodiazepines, though that really wasn’t an option, nor was it a long term solution, and it was far too early for the SSRI antidepressant to have kicked in fully. We encouraged them to stay the course with the antidepressant medication, and he could come back to see Dr. Annie in follow up in a month or two as we would have a much better idea at that point of how it was going to work and whether he needed a higher dose.
LJ evaluated a young patient who seemed to have hemifacial spasm – a disorder in which one half of the face begins to involuntarily twitch and can be very uncomfortable as well as impair function. It is believed to occur as a result of irritation of the facial nerve, often by a blood vessel that is in contact with the nerve and causes this mostly pure motor nerve to discharge frequently causing the spasm. It is perhaps the motor equivalent of another disorder, trigeminal neuralgia, that involves the trigeminal nerve, which is a pure sensory nerve of the face, leading to severe and disabling incredibly brief painful sensations that shoot through usually one or two divisions of the facial nerve distribution and is disabling. Trigeminal neuralgia, or tic douloureux as it used to be known, is one of two pains in neurology that are considered suicidal – the other being cluster headache.
The treatment for hemifacial spasm is essentially the same as for trigeminal neuralgia, being medications that make neurons less likely to fire spontaneously, such as when irritated, which are typically antiseizure medications, carbamazepine being the one most commonly used. The patient was placed on carbamazepine and instructed to return in one to two months to see Dr. Annie in follow up.
Natalie evaluated a young girl who she had seen briefly in the hospital several days prior for abnormal movements that were unlikely to be epileptic and were more concerning for some type of dyskinesia or dystonia. It turned out that her younger brother also had very similar movements, so they had both been asked to come to clinic to be seen by us. Both the children were otherwise normal developmentally and had normal neurological examinations, though they both described abnormal stiffening of their muscles, often precipitated by stress, that had been present since they were very young, making it very unlikely that this was a psychogenic problem. Based on the fact that both siblings had it (they also later described similar symptoms in an aunt), it was most likely a disorder with an autosomal dominant inheritance pattern and given their description of the episodes and the triggers, it was most likely paroxysmal nonkenisigenic dyskinesia, or PNKD. There is also a similar hereditary condition of paroxysmal kenisigenic dyskinesia, or PKD, in which the abnormal movements are triggered by sudden movements such as standing up. There is no cure for either of these disorders, though medications can help reduce the frequency of the episodes, and sodium channel blockers, such as carbamazepine or lamotrigine, are often used to reduce symptoms. As the older sibling was more significant affected, we opted to treat her with lamotrigine initially but would follow her and consider carbamazepine in the future if she was not responding to the initial medication.
We had decided to go out for a nice dinner at the Manor Lodge as it was Natalie’s last day at FAME – her husband and parents would be arriving tomorrow and they would all be traveling to the Crater and the Serengeti together for five days while we would be heading to the Serengeti first, but only for two nights so we would be missing running into each other by a day. The Manor Lodge sits high above Karatu and borders the Ngorongoro Conservation Area, so closely, in fact, that you have to pass through a short easement in the NCA to get to their gates. We have seen elephants and buffalo on the road before as we’ve passed through on our way to dinner which is just a little bonus. The Manor Lodge, which is operated by Elewana, a South African company, is one of the higher end lodges in Karatu and has always offered us a discount since we are working at FAME and helping the community. They have incredibly gorgeous grounds with views to equal, and their large cottages are designed to make one feel as though you were in the wine district of South Africa. The large Manor House is impeccably furnished with a lovely dining room, a large piano bar, and a downstairs media room for watching football matches.
We always arrive before sunset as the view to the west is fantastic and unless it’s horrible overcast, we’ve not been disappointed. Having drinks on their veranda is always special and tonight’s weather was perfect – there was a slight chill as the sun went down and the several nearby small chimineas were quickly lit to provide a hint of warmth before dinner. We were eventually called inside to a table that had more silverware than I think I have ever seen in East Africa (perhaps the Ngorongoro Crater Lodge that we stayed at two years ago may have equaled this). Dinner is a perfect five-course affair with smaller portions that are much preferred, and each course was amazing. LJ’s vegetarian dinner was equally delightful by report. The dining room was pretty much full, so we were very appreciative they were willing to accommodate us for the evening, and we spent two hours dining which meant that we weren’t rushed at all.
It was late when we started back down to Karatu, passing once again through the NCA easement, though we didn’t encounter any wildlife this time. We made a quick stop at the Golden Sparrow for a drink on the way home and arrived back home late with plans for three of us to leave early in the morning for the Serengeti and for Natalie to meet her family around lunchtime.