JSJonathan K. Smith

Jonathan K. Smith

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Jonathan K. Smith has a total of 27 co-authors. Here are the top co-authors by number of shared publications:

  • Mark E. Landau

    Walter Reed National Military Medical Center, Department of Neurology, American Bldg, 6th Floor, 9801 Rockville Pike, Bethesda, Maryland, 20889

    4 shared publications
  • Matthew E. Miller

    Department of Physical Medicine & Rehab, Walter Reed National Military Medical Center, Bethesda, Maryland, USA

    2 shared publications
  • Brett J. Theeler

    Department of Neurology, Walter Reed National Military Medical Center, Bethesda, Maryland, USA

    1 shared publication
  • Christina M. Cawley

    Department of Orthopedic Surgery, Walter Reed National Military Medical Center, Bethesda, MD, USA

    1 shared publication
  • Craig G. Carroll

    Walter Reed National Military Medical Center, Department of Neurology, American Bldg, 6th Floor, 9801 Rockville Pike, Bethesda, Maryland, 20889

    1 shared publication
  • David E. Reece

    Department of Physical Medicine and Rehabilitation, Walter Reed National Military Medical Center, Bethesda, Maryland USA

    1 shared publication

Latest Publications

  • Open Access

    Clinical Reasoning: A 26-year-old man with right hand and arm weakness

    by Emily J. Elliott, Jonathan K. Smith

    A 26-year-old infantryman developed right hand and arm weakness while deployed to Iraq. Extension of the right second digit worsened over 2 weeks, followed by difficulty extending digits 3-5 over the following weeks. He reported muscle twitching in the right upper extremity over the same period, and that his thumb would lock or cramp in an opposed position during use. He denied pain, motor, or sensory symptoms in other extremities. Nine months prior, he sustained an injury while parachuting during airborne school, resulting in a concussion, headache, and neck and back pain, but no weakness.

  • Nivolumab‐induced neuralgic amyotrophy with hourglass‐like constriction of the anterior interosseous nerve

    by Michael E. Porambo, Kaye E. Sedarsky, Emily J. Elliott, Brett J. Theeler, Jonathan K. Smith


  • Open Access

    Pathogenic and rare deleterious variants in multiple genes suggest oligogenic inheritance in recurrent exertional rhabdomyolysis

    by Nyamkhishig Sambuughin, Ognoon Mungunsukh, Mingqiang Ren, John F. Capacchione, Iren Horkayne-Szakaly, Kevin Chuang, Sheila M. Muldoon, Jonathan K. Smith, Francis G. O'COnnor, Patricia A. Deuster


  • High‐resolution ultrasound in combat‐related peripheral nerve injuries

    by Jonathan K. Smith, Matthew E. Miller, Craig G. Carroll, Walter J. Faillace, Leon J. Nesti, Christina M. Cawley, Mark E. Landau

    Introduction: Peripheral nerve injuries (PNI) sustained in combat are typically severe and are frequently associated with marked soft tissue damage, anatomic distortion, and retained metallic fragments. These features complicate clinical and electrodiagnostic assessment and may preclude MRI. Methods: We describe 4 cases of military personnel who sustained high‐velocity gunshot wounds or blasts with metal fragment injuries in which high resolution peripheral nerve ultrasound (US) proved beneficial. Results: In these cases, the clinical and electrodiagnostic exams provided inadequate localization and severity data of the nerve injuries, and MRI was either precluded or provided no additional information. In each case, US disclosed focal nerve segment abnormalities, including regions of focal enlargement and nerve discontinuity with end‐bulb neuroma, which guided surgical planning for nerve repair. The findings on US were subsequently confirmed intra‐operatively. Conclusions: High resolution peripheral nerve US is a useful modality in assessment of combat‐related PNI. Muscle Nerve, 2016 Muscle Nerve 54: 1139–1144, 2016


  • Iatrogenic Thenar Eminence Atrophy After Botox A Injection for Secondary Raynaud Phenomenon

    by Jeffrey C. Eickhoff, Jonathan K. Smith, Mark E. Landau, Jess D. Edison

    To the Editor Secondary Raynaud phenomenon (RP) is a vasospastic disease of digital arteries associated with various underlying connective tissue diseases. Symptoms range from pallor, cyanosis, and hyperemia to acral ulceration.1 Treatment typically involves behavioral modification and medications to encourage vasodilatory response and improve blood flow to tissues.2 Onabotulinum toxin A (BTX-A) injection is a non–Food and Drug Administration–approved novel therapy for management of refractory RP. Its mechanism of action includes blockade of vasoconstriction via inhibition of presynaptic acetylcholine (Ach) release and reduction in pain via decrease in nociceptors.3 Transient muscle weakness is a known adverse effect, but persistent atrophy is atypical.1 We report a patient with refractory RP who received BTX-A injections and developed persistent atrophy and weakness of the hand, illustrating a sustained adverse outcome from an emerging therapy for severe refractory RP. A 41-year-old woman with systemic lupus erythematosus (features include arthritis, photosensitivity rash, antinuclear antibody, and anti–double-stranded deoxyribonucleic acid antibody positivity, low complement) presented with a 10-year history of refractory RP that failed multiple medical trials including prazosin, diltiazem, vardenafil, tadalafil, sildenafil, and losartan. Symptoms at presentation were pallor, pain, and numbness of the distal fingers, occurring multiple times daily. Her regimen at presentation included topical nitroglycerine ointment, gabapentin, and aspirin 81 mg daily. She had no previous history of distal ulceration or tuft atrophy. Given her refractory symptoms, she was evaluated by an outside clinic and received BTX-A injection. For each digit of the right hand, two 10-unit doses of BTX-A were injected into the subcutaneous tissue overlying the neurovascular bundles, 1 cm proximal to the finger web, for a total of 100 U of BTX-A (Image 1, http://links.lww.com/RHU/A58). Two days later, she developed thumb weakness and difficulty in manual dexterity tasks. This was brought to clinical attention 11 days following BTX-A injection. She was initially managed expectantly given the normally transient weakness following BTX-A injection. The weakness persisted, and she then developed both clinical (Image 1, http://links.lww.com/RHU/A58) and radiographic (Image 2, http://links.lww.com/RHU/A59) evidence of thenar muscle atrophy. There was no symptomatic improvement of her Raynaud manifestations. Electrodiagnostic evaluation was performed 112 days following the BTX-A injection (Table 1). Median sensory studies were normal, but median motor studies demonstrated relatively decreased amplitudes. Repetitive nerve stimulation (RNS) at 3 Hz demonstrated a decremental response comparing the fourth stimulus to the first. There was no increase in the compound muscle action potential amplitude following voluntary exercise or RNS at 20 Hz. Needle electromyogram demonstrated abnormalities in median and ulnar innervated muscles. In occupational therapy, grip strength as measured by Jamar dynamometer, was 50/45/40-lb force on the right and 60/55/60-lb force on the left on 3 sequential tests. The lateral pinch, 3-jaw pinch, and tip pinch tests demonstrated asymmetry as well: right (0, 2, 0-lb force, respectively) and left (10, 8, 6-lb force, respectively). Two years after injection, the patient had functional improvement in pinch, grip, and handwriting exercises, but had not returned to premorbid levels of function. The clinical, electrodiagnostic, and radiographic features of this case support a causative role of BTX-A in induction of long-term weakness and atrophy. The temporal onset and location of weakness are consistent with typical manifestations of BTX-A treatment. The pattern of electrodiagnostic abnormalities excluded the possibility of a C8 or T1 radiculopathy, brachial plexopathy, or median nerve entrapment at the wrist (e.g.


  • Open Access

    Peripheral Nerve Ultrasound and Short-Segment Nerve Conduction Studies Before and After Ulnar Nerve Decompression

    by Jonathan K. Smith, Matthew E. Miller, David E. Reece, Yin-Ting Chen, Mark E. Landau, David E. Reece Do

  • Ethical considerations in elective amputation after traumatic peripheral nerve injuries

    by Jonathan K. Smith, Keith P. Myers, Robert G. Holloway, Mark E. Landau

    Summary Traumatic peripheral nerve injuries often complicate extremity trauma, and may cause substantial functional deficits. We have encountered patients who request amputation of such injured extremities, with the goal of prosthetic replacement as a means to restore function. Data on long-term outcomes of limb salvage vs amputation are limited and somewhat contradictory, leaving how to respond to such requests in the hands of the treating physician. We present example cases, drawn from our experience with wounded soldiers in a peripheral nerve injury clinic, in order to facilitate discussion of the ways in which these patients stress the system of medical decision-making while identifying ethical questions central to responding to these requests.