Transient Central Facial Palsy at High Altitude: A Case Report

Introduction

Besides commonly recognized forms of altitude sickness among which high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE) represent two life-threatening conditions, less is known about other altitude-related conditions (Bärtsch and Swenson, 2013; West et al., 2013). Among them, a peculiar cluster of neurological conditions that falls outside the definition of acute mountain sickness (AMS) has been reported in mountaineers for many years, varying from transient ischemic attacks (TIA) and strokes to cerebral venous thrombosis, migraine, or seizures (Basnyat et al., 2004; Richalet et al., 2020). Some of the neurological disturbances at high altitude are transient, whereas others are permanent. However, it is not clear if they are associated with AMS, HAPE, or HACE. The precise mechanisms involved in these neurological disorders at high altitude are still debated and their etiologies remain generally undetermined.

We present a case report of a transient neurological disorder at high altitude in a young woman during the descent after reaching the summit of Mount Kilimanjaro.

Case

A 34-year-old woman residing at low altitude made a 6-day ascent of Mount Kilimanjaro from September 30 to October 5, 2019. She had a history of thyroid carcinoma (treated by radical thyroidectomy, radiotherapy, and substitutive opotherapy), Raynaud's phenomenon, and endometrial cyst. She reported no history of migraine, and regularly trained for triathlons (8 hours/week) since 2012. She also had a family history of stroke and transient cerebral ischemia in her father, who had an episode at the age of 56.

Before her planned climb, she underwent a routine mountain medicine consultation, including clinical examination, resting electrocardiogram, and a hypoxia exercise test (Richalet et al., 2012; Canouï-Poitrine et al., 2014). Her risk factors were gender (female), regular endurance training, and rapid ascent profile, yielding of a calculated severe high-altitude illness score of 3.5. Following current recommendations, no acetazolamide was prescribed and safety advice was provided (i.e., avoid intense physical activity at the beginning of the stay >3,000 m, ensure good hydration, and be alert to the onset of altitude-related symptoms).

As part of a seven-member trekking group, she arrived in Tanzania with no opportunity for acclimatization. On day 1, she started the ascent through the Machame route from the Machame gate (1,790 m; 5,872 feet) to Machame Camp (2,980 m; 9,776 feet) and experienced sleep disturbance on the first night (numerous arousals, Lake Louise Score [LLS] = 2). On day 2 while ascending from Machame Camp to Shira Camp (3,650 m; 11,975 feet), she reported mild fatigue and persistent poor sleep during the second night (LLS = 3). On day 3, she left Shira Camp for the Lava Tower (4,650 m; 15,527 feet) and then descended to Barranco Camp (3,950 m; 12,960 feet). Her fatigue disappeared, but was replaced by mild headache and she continued to have poor sleep during the third night (LLS = 3). On day 4 she ascended from Barranco Camp to Barafu Camp (4,605 m; 15,109 feet) with additional symptoms compared with the previous day (i.e., day 3) of mild weakness and dizziness (LLS = 5). On day 5, she summited the Uhuru Peak (5,895 m; 19,341 feet) with increasing symptom intensity: moderate headache, nausea, moderate weakness and dizziness, and overall mild reduction in activity level (LLS = 8). After a stay of ∼30 minutes at the summit, she started her descent.

At Stella Point (5,756 m; 18,885 feet), she suddenly experienced visual blurring associated with tinnitus and severe almost incapacitating lightheadedness. Despite these symptoms, she did not alert the other members of the group and continued descending. She first stopped and sat down at an altitude of around 5,000 m because of persisting symptoms and finally alerted the leader of the group. While trying to drink water, she realized that she was not able to contract her lips and cheeks to swallow. A general medical practitioner member of the group proceeded with a clinical examination and noted a left flattened nasolabial fold associated with a fall of the left labial commissure. The physician also noted slight dysarthria, strong difficulties in whistling, and dysesthesia over the left lower face. Forehead wrinkles were symmetric and she was able to close her eyelids completely and no Charles Bell sign was present.

The group decided to continue the descent and had a short lunch around Barafu Camp (4,673 m; 15,331 feet) where her symptoms rapidly began to abate but with continuing moderate headache and lightheadedness. At arrival at Mweka camp (3,068 m; 10,066 feet), only mild headache persisted at the end of day 5. By morning of day 6, she was completely recovered and totally asymptomatic. When she returned home, she underwent complete medical examination with comprehensive testing. Blood tests were entirely normal, including a complete blood count, renal, liver, and thyroid functions. Hemostasis profile and lipid metabolism analysis were also within the normal range. Cerebral magnetic resonance imaging was normal without any signs of stroke.

Discussion

We report a case of moderate AMS (LLS = 8 at day 5) associated with transient central facial palsy occurring at high altitude with spontaneous and complete resolution during the descent of Mount Kilimanjaro.

Consideration of neurological problems at high altitude generally focus on life-threatening HACE, but many other neurological impairments have been previously reported. These neurological disorders at high altitude may accompany the progressive nonspecific symptoms of AMS that can possibly progress to HACE, but can also appear separately from altitude sickness. Even though the etiologies are uncertain, the high-altitude environment and the contribution of the substantial lack of oxygen are assumed to play a key role.

The two most probable diagnoses in our reported case were TIA and migraine. Numerous arguments suggest TIA considering the patient's age (34 years old, as most TIA at high altitude occur in younger people compared with lower altitude where TIA usually afflicts older people with cardiovascular risk factors) as well as the transient focal central facial palsy confirmed by a physician. Moreover, the patient had a history of Raynaud's phenomenon and a family history of stroke and TIA.

Even if the precise mechanisms involved in TIA at high altitude need to be further elucidated, it is highly likely that hypoxia leads to disturbances in vasomotor tone, particularly arterial vasospasm in the cerebral circulation. This physiological response to high altitude coupled with a personal and family history of cerebrovascular disease may have predisposed her to a transient episode of cerebral ischemia. Finally, the complete regression (within 2 hours) of her focal neurological manifestations and the absence of any abnormality on cerebral magnetic resonance imaging also support the diagnosis of a TIA.

Altitude is also known to trigger migraine attacks. Therefore, the second possible diagnosis is migraine with aura, based on the association of transient focal neurological impairment and headache. Indeed, it is still debated whether migraine and AMS share pathophysiological similarities. Thus, migraine should be considered in all patients presenting with headache and focal neurological disturbance at altitude (Utiger et al., 2002). Even though our patient experienced headache without describing the typical one-sided or pulsatile components of migraine, it is very difficult to distinguish migraine headache from that due to AMS (West et al., 2013). However, the absence of any history of migraine coupled with the lack of other symptoms such as photophonophobia leads us to consider that TIA was the most likely cause of her neurological presentation at very high altitude.

Conclusion

In the light of the described case and explorations performed after returning home, we hypothesized that this woman had moderate AMS along with a TIA at high altitude. It is generally believed that acute focal neurological impairment at high altitude occurs independently of altitude sickness and that only more global neurological disturbances develop early in the onset of HACE. However, AMS and focal impairment may also appear concomitantly, leading to the need to systematically consider all various diagnoses of neurological impairment occurring at high altitude.