Approach to the International Traveler With Neurological Symptoms

Kiran T Thakur; Joseph R Zunt


Future Neurology. 2015;10(2):101-113. 

In This Article

Weakness/Sensory Symptoms

Weakness or sensory symptoms are common neurological complaints in returning travelers. To narrow the broad differential diagnosis, it is important to determine whether both motor and sensory involvement occur together or in isolation. In addition, the timing and progression of symptoms, including any accompanying urinary or bowel symptoms, is critical. Distinguishing lower versus upper motor neuron pattern weakness on examination, and evaluation for a sensory level can be helpful for localization (spinal cord or peripheral nervous system). Below we discuss common etiologies of motor and sensory symptoms in travelers.

Schistosomiasis is predominantly a disease acquired in Africa, the Middle East, and Asia, and transmitted to humans by skin contact with freshwater populated by cercariae-infected snails.[72] Four species can infect humans, with Schistosoma mansoni most commonly associated with spinal cord involvement. Generalized pruritis commonly occurs soon after freshwater exposure, prior to the onset of neurological symptoms. Following infection, schistosoma penetrate the spinal cord by retrograde venous flow into the Batson vertebral epidural venous plexus, which connects the portal venous system to the spinal cord and cerebral veins. Neuroschistosomiasis typically presents as a flaccid paraplegia, sometimes associated with a sensory level and sphincter dysfunction, which then progresses to a spastic paraparesis.[73] Cerebral involvement may also occur, most commonly with Schistosoma japonicum. Some tourist destinations, such as the Dogon tribe's region of Mali, Banfora in Burkina Faso, the Omo National Park in Ethiopia and the southern shores of Lake Malawi, have been signaled in medical publications as areas of high risk though it is important to note that neurological manifestations in travelers remains rare.

As described above, encephalopathy is the most common neurological presentation associated with dengue, but patients may also present with weakness or sensory symptoms due to spinal cord or peripheral nerve involvement. Spinal cord involvement may occur during active infection, typically within 1–2 weeks after onset of systemic symptoms, or as a postinfectious immune-mediated phenomenon.[74–79] Neuroimaging and CSF analysis to detect intrathecal synthesis of dengue virus specific antibodies should be performed.[80] In addition, myalgias due to dengue infection are common but rarely progress to a fulminant myositis.[81] Elevated creatine kinase (CK) is commonly seen in patients who develop myopathic symptoms and should be closely monitored, as marked elevation suggests rhabdomyolysis.[82,83] Electromyography and muscle biopsy in patients with dengue typically reveal a paucity of findings.[84] Leptospirosis and Chikungunya have geographic and clinical overlap with dengue and should be considered in the differential diagnosis.

Rabies is most often transmitted to humans via the saliva of infected animals, usually dogs, and requires direct inoculation via a bite or salivary contact with mucous membranes.[85] The disease is endemic to countries on all continents except Antarctica, with most reported deaths occurring in children living in Africa and southeast Asia. As incubation periods can be highly variable, recent and remote history of a bite from a rabid animal should be elicited.[86] Rabies progresses from a nonspecific, prodromal phase with fever and vague symptoms, to the neurologic phase with initial symptoms of neuropathic pain or pruritis at the site of the bite. Other prodromal symptoms include generalized malaise, anxiety and spasms of swallowing muscles which can be stimulated by sight, sound or perception of water. Paralytic rabies accounts for approximately 30% of the total number of human cases, and presents with a clinical picture that resembles Guillain–Barre syndrome, with weakness initially developing at the site of the bite or scratch.[87] The actual rate of possible rabies exposure in travelers has not been calculated with accuracy. However, studies have found a range of roughly 16–200 per 100,000 travelers based on differing criteria.[88] Before travel, advice should include avoiding touching all animals, including wild animals and pets, as they may not be vaccinated against rabies. There should be vigilant supervision of children while they are in close proximity to dogs, cats and wildlife such as monkeys. Pre-exposure vaccination should be offered to people at high risk, such as laboratory staff working with rabies virus, veterinarians, animal handlers, wildlife officers, cave spelunkers as well as travelers taking excursions into rural locations with endemic rabies.[89] Post-exposure vaccination should be initiated immediately if a patient has been bitten by a rapid animal, regardless of symptoms at the time of evaluation.

Marine toxins found in contaminated seafood frequently produce neurological manifestations in returning travelers. With the substantial increase in seafood consumption worldwide, especially exotic raw seafoods consumed by tourists, the evaluating neurologist should be aware of potential serious neurological toxicity produced by these toxins. Paralytic shellfish toxicity is caused by saxitoxin and is associated with consumption of crustaceans, gastropods and fish in northwestern and northeastern USA, southern Chile and Japan.[90] Tingling or numbness begin periorally and spread to the neck and face, followed by headache, nausea, vomiting and diarrhea.[91] Death may result from respiratory muscle paralysis.[92] Diagnosis is based on clinical presentation and a history of seafood consumption in the preceding 24 h prior to symptom onset. Another toxin commonly encountered in sick tourists is ciguetera toxin, which produces gastrointestinal, neurological and cardiovascular symptoms.[93] More than 50,000 cases of ciguatera poisoning occur globally every year. The incidence in travelers to highly endemic areas has been estimated as high as 3 per 100 travelers.[94] Perioral paresthesias are common, and a reversal of temperature perception is nearly pathognomonic for this exposure; both symptoms may persist for several weeks. Neurotoxic shellfish poisoning is caused by members of the brevetoxin family of toxins, found principally in the Gulf of Mexico, Caribbean and New Zealand.[95] Symptoms include perioral paresthesias, diarrhea, gait deficits and the reversal of temperature sensation as is seen in ciguatera toxicity. Unlike ciguatera toxin, symptoms typically resolve within 48 h after onset and no deaths have been reported due to this illness.[96,97] No antidote exists for most of the neurotoxic marine toxins, and supportive treatment is the mainstay of therapy.