Diplejia braquial

OBSERVATION

Brachial Amyotrophic Diplegia in a PatientWith Human Immunodeficiency Virus Infection

Widening the Spectrum of Motor Neuron Diseases OccurringWith the Human Immunodeficiency Virus

Joseph R. Berger, MD; Patricio S. Espinosa, MD, MPH; John Kissel, MD

A lthough amyotrophic lateral sclerosis and progressive spinal muscular atrophy havebeen recognized to occur in association with human immunodeficiency virus infec-tion, to our knowledge, brachial amyotrophic diplegia, a form of segmental motor neu-ron disease, has not been previously reported. Brachial amyotrophic diplegia resultsin severe lower motor neuron weakness and atrophy of the upper extremities in the absence ofbulbar or lower extremity involvement, pyramidal features, bowel and bladder incontinence, andsensory loss. We describe a human immunodeficiency virusseropositive man without severe im-munosuppression or prior AIDS-defining illnesses who had brachial amyotrophic diplegia. Thisdisorder may represent one end of a spectrum of motor neuron diseases occurring with this ret-rovirus infection. ArchNeurol. 2005;62:817-823

Motor neuron disease associated with hu-man immunodeficiency virus (HIV) in-fection was first reported in 1985,1 4 yearsafter the initial description of AIDS. Clini-cal patterns of HIV-associated motor neu-ron disease may mirror those of amyotro-phic lateral sclerosis (ALS)1-5 or progressivespinal muscular atrophy (PSMA).6-11 How-ever, to our knowledge, a segmental formof PSMA referred to as brachial amyotro-phic diplegia (BAD) has not been previ-ously described in association with HIV in-fection. This disorder is a form ofneurogenic man-in-the-barrel syn-drome in which severe bilateral upper ex-tremity weakness is unaccompanied bybulbar lower extremity or pyramidal ab-normalities.12 When associated with mo-tor neuron disease, it has also been re-ferred to as the flail arm syndrome13 andthe hanging arm syndrome.14 BAD is clas-sified as a form of segmental lower motorneuron disease.15 While a similar clinicalphenotype of bilateral upper extremityweakness may occur following cere-bral,16-21 brainstem,22-24 cervical spinal

cord,25-28 or bilateral brachial plexus in-sult,29,30 these may be distinguished fromBAD by clinical presentation and radio-graphic and electrophysiological stud-ies.12 Furthermore, the lack of involve-ment of bulbar and lower extremitymuscles, the absence of pyramidal signs,and the long survival with this disorder dis-tinguish it from ALS.12,15 We describe anHIV-seropositive man presenting with pro-gressive upper extremity weakness that de-veloped in the absence of a detectable vi-ral load or any preceding AIDS-relatedcomplications.

REPORT OF A CASE

This 35-year-old man was first aware of aslowly progressive weakness of the rightshoulder in June 2000 when he noted dif-ficulty lifting heavy objects above his headwith his right arm. The symptoms in hisright arm progressed, and by June 2001,a similar weakness had developed in theleft shoulder. Weakness and wasting wereprogressive in both upper extremities andin his chest muscles in the ensuing months.He denied speech or swallowing difficul-ties, leg weakness, sphincter distur-

Author Affiliations: Departments of Neurology (Drs Berger and Espinosa) andInternal Medicine (Dr Berger), University of Kentucky College of Medicine,Lexington; and Department of Neurology, Ohio State University, Columbus(Dr Kissel).

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bances, fasciculations, or stiffness. He reported rare mildcramps in his right medial plantar muscles.

In February 2001, laboratory testing revealed that hewas HIV seropositive by enzyme-linked immunosor-bent assay and Western blot analysis. At that time, hisCD4 cell count was 244/L and his HIV viral load was8315 copies per milliliter. He started antiretroviral com-bination therapy, including zidovudine, lamivudine, andabacavir succinate (Trizivir) in August 2001, and by Sep-tember 2001, his CD4 cell count was 377/L and the HIVviral load was undetectable. His medical history was re-markable for diabetes mellitus diagnosed at the age of 14years, which had been complicated by diabetic retinopa-thy requiring a right eye vitrectomy in 1998, diabetic pe-ripheral neuropathy, and mild diabetic nephropathy withnonnephrotic proteinuria. The development of severeweakness of his upper extremities ultimately precludedself-injection of insulin, and an insulin pump was in-serted. There was no family history of neuromuscular dis-orders.

A physical examination performed in April 2003showed a slender man, weighing 55.8 kg. His cognition,language, and speech were normal. The result of a cra-nial nerve examination was normal. There was dramaticwasting of the muscles of the shoulder girdle and upperextremity and to a lesser extent the muscles of the fore-arms, hands, chest, and thorax (Figure). The scapulaewere winged. Coarse fasciculations were observed inmultiple muscles in the upper extremity and over thechest. His abdominal muscles were preserved. No spas-ticity was evident. Upper extremity strength was gradedas trace in both deltoids, 2 of 5 in the right biceps andbrachioradialis, 3 of 5 in the left biceps and brachiora-dialis, 4 of 5 in both triceps, and 4 of 5 at the wristextensors and flexors, although the extensors wereweaker. His interossei and other intrinsic hand muscleswere mildly weak. Wasting in the lower extremities wasconfined to both extensor digitorum brevis muscles,greater on the left, which was associated with weaknessof toe extension. Otherwise, strength in his lowerextremities was preserved. Muscle stretch reflexes weregraded as absent at the right biceps and brachioradialis,1 at the right triceps, trace at the left biceps and bra-chioradialis, 1 at the left triceps, 2 at both kneejerks, and trace at the ankles. There was no Hoffmannor Babinski sign, and his jaw jerk was normal. His gaitwas normal. Pinprick and temperature sensation werediminished to the lower third of the calves. Vibratoryand position sense was diminished in a stocking distri-

bution in the distal lower extremities, and the Rombergsign was positive.

The result of magnetic resonance imaging of the cer-vical spine was normal, with minimal degenerativechanges of the spine. With the exception of a mildlyincreased creatine kinase level (3.86105 U/L), theresults of hematologic and other laboratory studies,including erythrocyte sedimentation rate, rheumatoidfactor, antinuclear antibody, tests for hereditary neu-ropathy with liability to pressure palsies, and antibodiesto GM1 and myelin-associated glycoprotein, were nega-tive or normal. The complete blood cell count revealeda hemoglobin level of 12.3 g/dL, a hematocrit of 36%,and a white blood cell count of 6500/L, with a normaldifferential. The vitamin B12 level was 528 pg/mL (390pmol/L). Cerebrospinal fluid analysis showed 3/L leu-kocytes, 0 erythrocytes, a glucose level of 115 mg/dL(6.38 mmol/L), a protein level of 5.5102 g/dL, nega-tive microbiological study results, including those forthe VDRL test and cryptococcal antigen, normal cyto-logic test results, a normal IgG index, and 7 oligoclonalbands (attributed to HIV infection). Cerebrospinal fluidHIV viral assays were not performed. Electrophysiologi-cal studies performed on February 20, 2001, showedevidence of active and chronic denervation bilaterally ofmuscles innervated by C5 through the middle thoracicnerve roots by electromyography. The result of needleelectromyography of the lower extremities was normal,with the exception of the observation of long-durationlarge-amplitude motor unit action potentials, fibrilla-tion potentials, and mildly reduced recruitment in themuscles supplied by the superficial and deep peronealnerves. Nerve conduction studies in the legs revealedsensory amplitudes all greater than 60% of the lowerlimit of normal for our laboratory, with preserved con-duction velocities. Motor conductions were all greaterthan the 90th percentile of the lower limit of normal,with normal amplitudes. The changes overall werecompatible with a mild to moderate distal sensorimotorpolyneuropathy with predominantly axonal features.The findings on the nerve conduction study were com-plex and believed to be most consistent with diabeticperipheral neuropathy, a right peroneal neuropathy,and bilateral mild ulnar nerve entrapments at theelbow.

A trial of intravenous immunoglobulin was initiatedin October 2003 without any improvement. ThroughJanuary 2004, there was neither significant progressionof his weakness nor development of any cranial nerve ab-normalities or weakness, cramps, or fasciculations of thelower extremities.

COMMENT

Motor neuron disease with HIV infection may appear inseveral forms. A summary of previously reported casesof motor neuron disease complicating HIV infectionand a summary of our patient are included in theTable. Motor neuron disease with HIV infection maybe indistinguishable from classic ALS, resulting in aninexorably progressive disorder of upper and lower

Figure. Profoundwasting of the musclesof the upper extremitiesand chest is evident.




Table. Summary of Cases of Motor Neuron Disease Heralding HIV Infection

SourceAge, y/Sex

ClinicalManifestations

CD4 CellCount/L Viral Load at Dx CSF Findings

OpportunisticIllness Treatment Outcome Survival

Zoccolella etal,5 2002

44/M CC: hand weakness,cramps, andweight loss. NE:hypotrophy andfasciculations(tongue andupper and lowerlimbs); nosensoryabnormalities;Hoffman andBabinski signspresent.

360 34 000copies/mL

Leukocytes,7/L; glucose,43 mg/dL;protein,6.1 10-2

g/dL; HIVRNA, 370copies/mL

None Zidovudine,lamivudine, andnevirapine

Bedridden,respiratoryfailure, death

3 y

Nishio et al,6

200142/F CC: dysphagia,

dysarthria, anddysphonia. NE:hypotrophy andfasciculations(tongue) andproximal limbweakness andatrophy; nosensoryabnormalities.

107 44 510copies/mL

Leukocytes,29/L;glucose, 46mg/dL;protein,12.6 10-2

g/dL

None Stavudine,lamivudine, andnelfinavir mesylate

Improvementof thesymptomsafter therapy,alive

Alive, minimalneurologicalproblems?

Verma et al,9

199032/M CC: progressive

lower limbweakness pluscramps. NE:upper and lowerlimb proximalweakness andfasciculations;mild atrophy; nosensoryabnormalities.

NA (T4/T8,0.73)

NA NA None at Dx NA Successiveopportunisticinfections,death

2 y

Casado etal,4 1997

30/M CC: progressiveupper limbweakness plushypotrophy. NE:upper and lowerlimb distalweakness andfasciculations;mild atrophy; nosensoryabnormalities.

NA (T4/T8,0.76)

NA Normal None NA Deterioration ofPSMA Sx,HIV infection,stable

Alive atpublication

Galassi etal,7 1998

30/M CC: extremityweakness,cramps, weightloss, and fatigue.NE: proximal limbasymmetricweakness; flexorplantar response;mild atrophy; nosensoryabnormalities.

340 (T4/T8,0.4)

NA Leukocytes,0/L; glucose,NA; protein,17.4 10-2

g/dL

Skin bacterialinfections

Zidovudine,zalcitabine, andmethylpredniso-lone

Progressiverespiratoryfailure, death

NA

Sastre-Garriga etal,31 2000

39/F CC: lower limbweakness andcramps. NE:hypotrophy andfasciculations(tongue); distallimb weakness;no sensoryabnormalities.

540 NA Leukocytes,0/L; glucose,60 mg/dL;protein,2 10-2 g/dL

NA NA NA NA

(continued)




Table. Summary of Cases of Motor Neuron Disease Heralding HIV Infection (cont)

SourceAge, y/Sex




MacGowanet al,2

2001

32/F CC: generalizedweakness, weightloss, anddysarthria. NE:tonguefasciculations andupper and lowerlimb proximal andmore distalweakness;Hoffman andplantar signspresent; nosensoryabnormalities.

44 77 900copies/mL

Leukocytes,14/L;glucose, NA;protein,13.4 10-2

g/dL

None Zidovudine,lamivudine, andnelfinavir

Deterioration;and afterantiretroviraltreatment, fullrecovery

Alive

Goldstein etal,32 1993

22/F CC: lower extremitypain andweakness. NE:upper limb P/D,4/5; distal limb P,3/5, D 2/5; mildsensoryabnormalities.

438 (T4/T8,0.39)

NA Leukocytes,1/L; glucose,NA; protein,7.3 10-2

g/dL

None Zidovudine, IVimmunoglobulin,andmethylpredniso-lone

Deterioration,relapses,improvement

NA

38/M CC: facial droopand upper limbweakness. NE:upper and lowerweakness; DTRabsent; nosensoryabnormalities.

353 (T4/T8,0.45)

NA Leukocytes,16/L;glucose, NA;protein,15 10-2

g/dL

None IV immunoglobulin,methylpredniso-lone, andplasmapheresis

Deterioration,stabilization

NA

Huang etal,10 1993

45/M CC: generalizedweakness,fasciculations,weight loss, andquadriplegia. NE:tongue atrophyandfasciculations;upper and lowerlimb paralysis; nosensoryabnormalities.

397 (T4/T8,1.13)

NA Leukocytes,11/L;glucose, 60mg/dL;protein,5.7 10-2

g/dL

None Zidovudine No furtherdeterioration

NA

Moulignieret al,3

2001

27/M CC: right handweakness, musclewasting, anddysarthria.

84 NA Leukocytes,5/L; protein,4.6 10-2

g/dL

None Zidovudine Transientstabilization

6 mo (ADC)

61/M CC: left legweakness, musclewasting, andcramps.


g/dL

None Zidovudine Full recovery 2 y (OI)

29/M CC: left legweakness andtonguefasciculations.


g/dL

None Zidovudine Partial recovery Unknown(unavailableforfollow-up)

22/M CC: bilateral lowerlimb weakness,muscle wasting,andfasciculations.

37 3.7 log10

copies/mLLeukocytes,

13/L;protein,5.2 10-2

g/dL

None Zidovudine anddidanosine

Partial recovery 3 y (OI)

25/M CC: left armweakness, musclewasting, andfasciculations.

123 4.9 log10


2/L; protein,3.6 10-2

g/dL

None Zidovudine andzalcitabine

Partial recovery 4 y (ADC)

40/F CC: left armweakness andmild muscleatrophy.

227 3.3 log10


1/L; protein,4.2 10-2

g/dL

None Zidovudine anddidanosine

Full recovery Alive for3 y

(continued)




motor neurons.1-5 Alternatively, progressive lowermotor neuron disease affecting bulbar and extremitymuscles may occur in the absence of upper motor neu-ron findings consistent with PSMA.6-11 Other disordersoccurring with HIV infection that mimic motor neurondisease include chronic inflammatory polyradiculoneu-ropathy,34 axonal motor polyradiculoneuropathy,32 andmultifocal motor neuropathy with anti-GM1 antibod-ies.33 While progressive lower motor neuron weaknessis seen with these disorders, the slow tempo of ourpatients illness would be distinctly unusual for chronicinflammatory polyradiculoneuropathy and multifocalmotor neuropathy, and its severity and distributioninconsistent with HIV-associated axonal motor polyra-diculoneuropathy.

Our patient had focal weakness of the right upper ex-tremity that progressed to involve the left upper extrem-ity during the ensuing year. The weakness and wastinghave remained confined to a few myotomes of the cer-vical and upper thoracic region. There has been neitherinvolvement of bulbar muscles nor progressive weak-ness of his lower extremities. The lower extremity find-ings of distal sensory loss, depressed ankle jerks, and dis-tal wasting and weakness are the consequence of hisconcomitant diabetic peripheral neuropathy and mild en-trapment neuropathies. Therefore, we believe that pro-found weakness and wasting of his upper extremities areconsistent with BAD.

Diabetes may result in brachial and lumbosacralplexopathies, resulting in a disorder referred to as dia-

betic radiculoplexus neuropathy (or diabetic amyotro-phy) that may mimic the disorder observed in our pa-tient.35 This disorder, however, affects the lumbosacralplexus in most cases, and upper extremity involvementis uncommon.36,37 In addition, patients with brachial dia-betic radiculoplexus neuropathy typically have unilat-eral weakness that progresses more rapidly than in ourpatient with preceding weight loss, severe pain, and sen-sory and autonomic abnormalities.35 Because none of thesefeatures was present in our patient, we think this an un-likely cause of our patients disorder.

Motor neuron disease occurring in association withHIV infection has been attributed to direct damage to themotor neurons by HIV, neurotoxic HIV viral proteins,cytokines and chemokines arising consequent to HIV in-fection, and opportunistic viruses that directly attack mo-tor neurons.32 The prototypical virally mediated motorneuron disease is poliomyelitis36; however, it is clini-cally quite distinct from the inherited and idiopathic formsof motor neuron disease. Flaccid paralysis has been re-ported with various viruses in the Enterovirus genus.36

Recently, French investigators have found the nucleic acidof enteric cytopathogenic human orphan virus, an en-terovirus, in the neuronal cell bodies within the gray mat-ter of the spinal cord of 88% of patients with ALS, sug-gesting a possible association between this enterovirusand ALS.37 However, poliovirus and other enterovi-ruses, when associated with weakness, are typically char-acterized by an acute febrile illness followed by a flaccidparalysis of 1 or more limbs.36 Whether HIV infection it-

Table. Summary of Cases of Motor Neuron Disease Heralding HIV Infection (cont)

SourceAge, y/Sex




Hoffman etal,1 1985

26/M CC: weakness,atrophy, andfasciculations ofthe left arm.

NA NA NA None NA Progressive 1 y

Sher et al,8

198830/M CC: weakness,

wasting, andfasciculations.

NA NA NA None NA Partial recovery 3 mo(pneumonia)

Simpson etal,33 1994

45/M CC: asymmetriclimb weakness,atrophy, andfasciculations.

560 NA NA None Zidovudine,prednisone, and IVimmunoglobulin

Stabilization 24 mo(opportunis-ticinfections)

Presentcase

35/M CC: weakness(upperextremities). NE:atrophy ofshoulder girdle,upper proximalextremities, andpectoral andthoracic muscles;mild sensoryabnormalities dueto concomitantdiabeticneuropathy.

244 Undetectableviral load

Leukocytes,3/L; glucose,115 mg/dL;protein,5.5 10-2

g/dL;oligoclonalbands, 7

None Zidovudine,didanosine,abacavir succinate,and IVimmunoglobulin

Stabilization,no furtherdeterioration

Alive 46 moafter onset

Abbreviations: ADC, AIDS dementia complex; CC, chief complaint; CSF, cerebrospinal fluid; D, distal; DTR, deep tendon reflex; Dx, diagnosis; HIV, humanimmunodeficiency virus; IV, intravenous; NA, data not available; NE, neurological; OI, osteogenesis imperfecta; P, proximal; PSMA, progressive spinal muscular atrophy;Sx, symptoms; T4/T8, ratio of CD4 to CD8 lymphocytes.

SI conversion factor: To convert glucose to millimoles per liter, multiply by 0.05551.




self or an accompanying, currently unrecognized, op-portunistic infection is responsible for the motor neu-ron findings in HIV-infected persons with motor neurondisease or whether it is unrelated to HIV infection re-mains to be determined. Findings of reverse transcrip-tase,38 antibodies directed to human retroviral anti-gens,39 an association of human T-lymphotropic virus Iwith clinical and pathological features consistent withALS,40,41 amplification of human T-lymphotropic virustax/rex,39 animal models of retrovirus-induced motor neu-ron disease,42,43 and the presence of PSMA and ALS inHIV infection suggest that HIV infection is causative orcontributory.

While the pathogenesis of ALS remains a conun-drum, several theories have been proposed. Among thepossible mechanisms that are considered are neuronalexcitation and free radical generation.44 Both of thesemechanisms have also been proposed as pathways to brainneuronal injury in the setting of HIV infection.45 Mito-chondria, through several mechanisms, have also beensuggested as instrumental in ALS, as in other neurode-generative disorders.46 A critical role of the mitochon-dria in neuronal apoptosis has been suggested with neu-rotoxic HIV proteins, gp120,47 and Tat.48 Someinvestigators have also advanced a role for autoimmu-nity in ALS.49,50 Antineuronal antibodies have been dem-onstrated in HIV infection, and may correlate with thepresence of dementia.51,52 Therefore, several proposedpathogenetic mechanisms for ALS may also be opera-tive in HIV-associated central nervous system disease.

In conclusion, motor neuron disease occurs in asso-ciation with HIV infection. The spectrum of HIV-associated motor neuron disease is broad and includesBAD, PSMA, and ALS. These disorders remain rare, andtheir underlying pathogenesis is uncertain.

Accepted for Publication: June 16, 2004.Correspondence: Joseph R. Berger, MD, Department ofNeurology, University of Kentucky College of Medi-cine, 740 S Limestone St, Lexington, KY 40536-0284([email protected]).Author Contributions: Study concept and design: Bergerand Kissel. Acquisition of data: Berger and Kissel. Analy-sis and interpretation of data: Berger and Espinosa. Draft-ing of the manuscript: Berger and Espinosa. Critical revi-sion of the manuscript for important intellectual content:Berger and Kissel. Administrative, technical, and materialsupport: Berger and Espinosa. Study supervision: Berger.

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