although spinal cord abnormalities in patients with acquired immunodeficiency syndrome ( aids ) have been infrequently reported in the literature , myelitis is a known complication of aids and is occasionally the initial complaint
. the incidence of myelopathy may be as high as 20% , with 50% of the cases reported post - mortem [ 3 , 5 ] .
toxoplasmosis is the most common cause of intracranial lesions responsible for neurological deficits in aids patients , occurring in 310% of patients in the united states and in up to 50% of aids patients in europe , latin america , and africa [ 6 , 10 ] .
a review of existing literature suggests that although toxoplasmic myelitis is uncommon , it should be suspected in immunocompromised patients who present with symptoms of acute or sub - acute myelopathy .
the initial evaluation should aid in differentiating between other reported causes of myelopathy ( such as vacuolar myelopathy , lymphoma , tuberculosis , and viral infections including cytomegalovirus infection , herpes zoster , and herpes simplex ) in aids patients [ 2 , 4 ] .
since 1986 , 18 cases of apparent toxoplasmosis of the spinal cord have been described [ 4 , 7 , 11 , 12 ] .
a case report and pertinent literature were reviewed , leading to the diagnosis and management options discussed below .
a 40-year - old hispanic man was admitted to the hospital after being found unconscious . he had a 2-day history of disorientation that manifested itself as his being unable to recognize family members . upon admission he regained consciousness , becoming alert and oriented , but developed urinary retention and was unable to move or feel his lower extremities .
he had no history of systemic illness , but mentioned having been treated for herpes zoster approximately 3  years prior .
he denied having a history of fever , chills , nausea , vomiting , rash , seizures , or other constitutional symptoms .
he had not traveled recently , and his hiv status was unknown at the time of admission .
physical examination revealed fever , nuchal rigidity , and a distended bladder that required catheterization .
a neurological examination confirmed that he had intact cranial nerves and normal upper extremity strength .
both lower extremities exhibited flaccid paralysis and reduced response to pain , touch , and temperature ( bilaterally from l1 ) .
cerebellar examination was normal in the upper extremities , with an adequate finger - to - nose exam .
the patient s wbc , hemoglobin , platelets , electrolytes , bun , and creatinine were within normal ranges on admission .
the initial brain ct ( without contrast ) revealed a focal area of vasogenic edema in the left frontal lobe ( without significant mass effect ) and abnormal white matter hypo - density seen along the lateral aspect of the right frontal horn of the internal capsule .
a brain mri ( with and without gadolinium enhancement ) revealed multiple bilateral ring - enhancing intra - axial brain lesions , and an ill - defined cortical and sub - cortical enhancement , with diffuse edema in the frontal lobe . spinal mri ( with and without gadolinium ) showed the spinal cord to be abnormally diffuse , with swelling and edema in the cervicothoracic region . along with the diffuse abnormal hyperintense swelling ,
the cauda equina had an edematous appearance , and signal intensity was abnormally increased , which is compatible with transverse myelitis ( figs .  1 and 2 ) .
finally , imaging also revealed a focal area of abnormal signal intensity in the ventral inferior pons . 

1initial mri : notice the abnormal spinal cord swelling cervical and at cauda equinafig . 
2normal f / u study initial mri : notice the abnormal spinal cord swelling cervical and at cauda equina he was initially given broad spectrum antibiotics ( ceftriaxone , vancomycin , and ampicillin ) and acyclovir at admission for a presumptive cns infection .
hiv serology was recommended , though the patient denied ever having engaged in high - risk behavior or having had a blood transfusion at any time in his past .
analysis of csf showed abnormal values including a wbc count of 11/mm and a protein level of 184.5  mg / dl , with a glucose concentration of 51  mg / dl .
stain and cultures for bacteria , fungi , and acid - fast bacilli were negative . a csf cryptococcal antigen titer and htlv i
an anti - toxoplasma immunoglobulin ( igg ) immune titer was positive at 8.99 ( < 0.9  =  negative ; 1.10  =  positive ) .
at this point , the patient disclosed having engaged in homosexual behavior and accepted hiv testing , which was reactive by elisa .
empiric treatment for toxoplasmosis with sulfadiazine , pyrimethamine , folinic acid , and haart therapy with lamivudine / zidovudine and indinavir were started .
intravenous dexamethasone was administered for 7  days , and oral methylprednisolone for another week .
biopsy was deferred due to possible complications and the evidence of improvement with therapy . within 4  days of empiric treatment for toxoplasmosis , the patient s neck rigidity resolved .
he progressively developed discrimination to touch and his vibratory sensation improved , as did his bilateral strength ( 1/5 ) of the lower extremities .
follow - up consisted of a brain and spinal cord mri ( with and without gadolinium ) , 14  days after treatment with anti - toxoplasmosis therapy combined with steroids , which demonstrated resolved swelling and residual t2 hyper - intensity in the mid - thoracic spinal cord , without an interval change in the brain mri .
aids - related spinal cord disorders include neoplasms , infections ( including hiv itself ) , vascular disease , and other undefined etiologies .
toxoplasmosis and lymphoma are the two most common intracranial lesions , and both have been reported in increasing frequency in the spinal cord .
myelopathy is usually under - diagnosed , probably because of the occurrence of coexisting conditions such as aids dementia complex ( adc ) , cerebral lesions of varying etiologies , vacuolar myelopathy , lumbosacral myelopathy , or peripheral neuropathy that may mask the clinical signs suggestive of myelopathy [ 5 , 9 , 10 ] .
other causes of myelopathy appear to be less common than toxoplasmosis and include tuberculoma , cytomegalovirus , varicella - zoster virus , and , possibly , lymphoma [ 4 , 10 ] .
postmortem histopathology examination has resulted in a definitive diagnosis of myelopathy in the majority of patients .
spinal cord lesions often manifest with a variety of symptoms , such as leg weakness , progressive paraparesis with spasticity , absent reflexes , ataxia , incontinence , and paresthesias . in the 14 toxoplasmosis cases with spinal cord involvement reviewed by vyas and ebright
, they found the most common presentations of acute or sub - acute symptoms were paraparesis , urine retention , sensory level deficits , fever , and local pain .
csf cytology showed increased protein - level elevation and a cd4 count of less than 50/mm . in the patients evaluated by spinal cord mri imaging , localized intramedullary lesions or spinal cord edema
were found in more than 90% of cases associated with positive t. gondii igg antibody .
no cases of associated transverse myelitis , as in this case , were described . in our case ,
evaluation in a symptomatic patient should include serum and csf cytology and antibody ( immunological ) studies as they remain the gold standard for identifying an infectious agent .
complete radiographic imaging of the entire neuroaxis [ 3 , 15 ] is key in clearly defining inflammatory lesions of the brain and spine , and in the visualization of typical lesions that allow for rapid diagnosis .
this helps determine whether the lesion is extramedullary or an intrinsic spinal cord disease , which in turn provides information to determine whether surgical or medical therapy is needed . in opportunistic diseases , the imaging studies also have a crucial role in diagnosis and monitoring of the therapeutic response . neuroimaging findings , along with other clues , help to narrow the differential diagnosis . on an mri , findings of a normal - sized spinal cord but with an abnormal signal should signal the possibility of vacuolar myelopathy and adc - related hiv myelitis .
lesions of viral myelitis can potentially cause spinal cord enlargement ; however , laboratory data are required for confirmation .
if spinal cord enlargement is present , toxoplasma myelitis and lymphoma should be strongly considered .
lymphoma has been associated with positive csf polymerase chain reaction ( pcr ) for epstein - barr virus .
if both spinal cord enlargement and an abnormal signal are associated with meningeal enhancement , then cmv , m. tuberculosis , lymphoma , and toxoplasmosis should be considered along with other less likely infectious causes .
mri ( plain and contrast - enhanced ) is currently considered appropriately sensitive for detecting brain and spinal cord lesions ; however , equal sensitivity has been reported using delayed - contrast ct scanning .
the current guidelines for diagnosis of intracranial lesions state that t1 spect is an option when available . when positive ( marked uptake in contrast to toxoplasma ) , it appears to be highly specific for primary cns lymphoma [ 6 , 8 ] .
these guidelines have been described as helpful   in spinal cord lesions and suspected lymphoma , although specific guidelines for spinal cord lesions are not presently available .
the newer and more available mri techniques of diffusion - weighted imaging ( dwi ) may be of help in the differentiation of lymphoma , showing no restriction in water diffusion .
if a diagnosis of solitary or atypical lesions can not be made with noninvasive methods , a biopsy ( open or stereotactic ) may be warranted in patients with concomitant negative toxoplasmosis serology since a negative serology does not exclude diagnosis of toxoplasmosis nor differentiate from lymphoma . a biopsy
may also be considered necessary if a patient experiences a rapid decline in function or , alternately , fails to improve despite therapy .
brain biopsies have been associated with hemorrhage risk and an increased mortality ( 2% ) and morbidity rate ( 12% ) in patients with hiv / aids .
empiric treatment for toxoplasmosis with oral pyrimethamine and sulfadiazine ( with folinic acid ) has been recommended in all cases of intracranial mass lesions in patients with hiv / aids ( except in a solitary mass with negative toxoplasma serology ) .
steroids promote radiological improvement in about 80% of patients , and improvement can be seen in about 1  week , supporting the diagnosis .
patients are usually monitored clinically and radiographically for response to treatment over a 10- to 14-day period following empiric therapy .
if responsive , anti - toxoplasmosis therapy is continued indefinitely , and reevaluation in the absence of steroid treatment is mandated . if the lesions remain unchanged or progress , the diagnosis has to be reconsidered and the therapeutic strategy reevaluated . in cases of atypical large solitary toxoplasma lesions resembling lymphoma ( that also present with spinal cord enlargement ) , additional diagnostic modalities should be performed [ 3 , 6 ] . due to the immunosuppressant effects of steroids ,
the optimal dosage and period of treatment for spinal cord lesions must be addressed in future studies . in this case , the brain and spinal cord lesions were found in an hiv - positive man who had not previously been diagnosed .
for this reason , other causes of cns infection and lymphoma were first considered . after the positive serology , empiric treatment for cerebral toxoplasmosis was initiated .
the patient s clinical and radiographic improvement led to the final diagnosis of toxoplasmic myelitis and encephalitis , similar to other cases documented in the literature by vyas et al . in 1996 .
furthermore , toxoplasmic myelopathy has been described in patients without hiv , albeit with severe immunosuppression [ 2 , 3 , 11 , 12 ] , and in patients with isolated spinal cord lesions [ 1 , 2 , 11 ] .
new neurological deficit in any patient should raise a high index of suspicion of hiv infection .
appropriate diagnostic methods and management that are practical for all settings , including those with limited technologies , should be sought .
newer methods of diagnosis and management for all neurological complications of hiv should be addressed .
we established ours based on the clinical manifestations , history , and general improvement of the patient 's condition .
although spinal cord toxoplasmosis is uncommon , it has been suggested that most patients with aids that present with evolving myelopathy , characterized by extremity weakness , sensory involvement , spinal cord enlargement , and enhancing lesions in brain or spinal cord ct or mri , have toxoplasmic myelitis [ 3 , 5 ] .
the likelihood of diagnosis increases if serum titers for toxoplasma antibodies are positive or where the initiation of early treatment with empiric anti - toxoplasmosis therapy and steroids improves both the patient s clinical and radiographic manifestations .
 approximately 10% of patients with aids present with some neurological deficit as their initial complaint , and up to 80% will have cns involvement during the course of their disease . 
 toxoplasmosis is the most common cause of cerebral mass lesions in patients with aids , but appears to be an uncommon cause of spinal cord disease . 
 the incidence of myelopathy may be as high as 20% , with 50% of the cases reported post - mortem . 
 we present a unique case of spinal cord disease as the initial presentation of aids . 
 we also present a comprehensive literature review of this topic , its diagnosis and treatment . 
 this is a retrospective chart review case report . after a detailed case presentation , 
 several diagnostic and therapeutic aspects of this unique case are thoroughly discussed . 
 although spinal cord toxoplasmosis is uncommon , it has been suggested that most patients with aids that present with evolving myelopathy , characterized by extremity weakness , sensory involvement , spinal cord enlargement , enhancing lesions in brain or spinal cord ct or mri , have toxoplasmic myelitis . 