Peer Reviewed

Photo Essay

A Collection of Complications Related to Drugs or Devices

Intermittent Coma in a Patient With an Intracranial Intrathecal Baclofen Pump Catheter

Kathleen E. Knudson, MD, and Donald C. Shields, MD, PhD
The George Washington University, Washington, DC


Our patient was a 66-year-old woman who had previously received diagnoses of multiple sclerosis in 1992 and Parkinson disease in 2004. She had developed progressively worsening spasticity that had left her wheelchair-bound for the past 5 years.

History. For her spasticity, she had undergone placement of an intrathecal baclofen pump by an unaffiliated surgeon. After placement of the baclofen pump, she stated that her spasticity had improved. However, she also began to develop episodes of somnolence, wherein she became unarousable for 6 to 12 hours. Per witnesses, she could not be awakened even with vigorous, painful stimuli during these episodes; then, she would awaken as if from sleep. When these episodes first occurred, she had been taken to the local emergency department on multiple occasions, but no etiology could be ascertained. Later, these episodes became progressively more frequent, occurring almost weekly.

Physical examination. On examination, she showed evidence of spasticity and increased tone in her upper and lower extremities without fasciculations or abnormal movements. The remainder of the neurologic examination findings were unremarkable.

Diagnostic tests. A computed tomography (CT) scan of the head (Figure) showed the intrathecal baclofen pump catheter terminating ventral to the brainstem, at the level of the pons, just posterior to the clivus. There was no prior imaging available from the initial surgery to determine whether this was the original placement or whether the catheter had migrated. After discussion with the patient of the risks and benefits of surgical intervention, the patient elected to undergo surgical retraction of the catheter.

Figure. Noncontrast head CT with sagittal reconstruction showing the intrathecal baclofen pump catheter tip in the CSF space ventral to the brainstem.


During surgery, C-arm fluoroscopy was used to visualize the catheter tip. The prior surgical site on her back was opened, and the sutures holding the catheter anchor were cut. We retracted the catheter gently under direct fluoroscopic guidance; it moved freely without evidence of tethering. The tip was retracted to the level of C7 vertebra, and a second anchor was sutured in place to prevent migration.

Outcome of the case. The patient was followed closely as an outpatient after her surgery. She had 3 short episodes of somnolence within the first month after surgery; however, she did not have any further episodes for the following 12 months. She continued to report good relief of her spasticity, and neurologic examination findings remained unchanged from those of the preoperative examination. Postoperative radiographs revealed stable position of the catheter tip at the cervicothoracic junction.

Discussion. Intrathecal baclofen has been increasingly used for the treatment of spasticity in children and adults. It has been shown to reduce spasticity and contractures and improve functional ability. However, complications associated with the surgical procedure, device, or drug have been reported.1 The most common complications are infection, hematoma, and cerebral spinal fluid (CSF) leak.2 Complications related to the catheter commonly are catheter migration, kinking, disconnection, or breakage. Catheter-related complications are most common within the first year of implantation.2 

Common complications related to the pump are rare and are largely due to misplacement or migration of the pump. To our knowledge, this is the first report of a patient with symptoms from a baclofen pump catheter tip that was found at the level of the brainstem.

A definitive explanation for our patient’s episodes of somnolence remains unclear. Similar episodes of temporary coma have been reported rarely. Anderson and colleagues3 reported delayed postoperative coma in 5 children following surgery for insertion of an intrathecal baclofen pump. They suggested that the cause of these episodes was likely inadvertent administration of an intrathecal baclofen bolus. In our patient’s case, there was no evidence of her having received intrathecal baclofen boluses prior to symptom onset, but the location of the catheter tip allowed for possible mechanical trauma and delivery of more-concentrated medication in the vicinity of the brainstem. Of note, baclofen pump catheters have since been placed in the cervical spine4 and intraventricular space5 without provocation of somnolence or unresponsiveness.


  1. Borrini L, Bensmail D, Thiebaut J-B, Hugeron C, Rech C, Jourdan C. Occurrence of adverse events in long-term intrathecal baclofen infusion: a 1-year follow-up study of 158 adults. Arch Phys Med Rehabil. 2014;95(6):1032-1038.
  2. Motta F, Antonello CE. Analysis of complications in 430 consecutive pediatric patients treated with intrathecal baclofen therapy: 14-year experience. J Neurosurg Pediatr. 2014;13(3):301-306.
  3. Anderson KJ, Farmer JP, Brown K. Reversible coma in children after improper baclofen pump insertion. Paediatr Anaesth. 2002;12(5):454-460.
  4. Ughratdar I, Muquit S, Ingale H, Moussa A, Ammar A, Vloeberghs M. Cervical implantation of intrathecal baclofen pump catheter in children with severe scoliosis. J Neurosurg Pediatr. 2012;10(1):34-38.
  5. Turner M, Nguyen HS, Cohen-Gadol AA. Intraventricular baclofen as an alternative to intrathecal baclofen for intractable spasticity or dystonia: outcomes and technical considerations. J Neurosurg Pediatr. 2012;10(4):315-319.

NEXT: Pityriasis Lichenoides et Varioliformis Acuta Exacerbated During a Course of Isotretinoin

Pityriasis Lichenoides et Varioliformis Acuta Exacerbated During a Course of Isotretinoin

John E. Jackson, MD, and Adam Perry, MD
United States Navy


The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the US Navy or the US Department of Defense at large.


A 25-year-old woman presented to the clinic 1 week after having initiated isotretinoin treatment for cystic acne. She had noticed a rapid progression of erythematous papules covering her legs, buttocks, and arms after a short preceding interval during which 5 similar papules had appeared on her upper extremities. She had noticed these initial 5 papules during a 1-week period in which she had stopped oral tetracycline in preparation for beginning isotretinoin therapy. She denied any personal or family history of similar dermatoses.

Physical examination. Physical examination showed more than 50 erythematous papules with occasional crusting on her lower extremities, buttocks, and inner arms but sparing her trunk and back (Figures 1 and 2). There were no associated systemic symptoms, recent illnesses, or fevers.


Diagnostic tests. The patient’s laboratory study results showed no evidence of abnormalities; specifically, liver and renal function were normal, with negative HIV and Epstein-Barr serology results.

Two representative lesions were chosen for punch biopsy and sent for pathologic analysis. Histology results of the specimens showed lymphocytic vasculopathy associated with interface dermatitis, along with evidence of confluent parakeratosis, perivascular lymphocytes and lymphocytic infiltration along the dermoepidermal junction associated with extravasated red blood cells (Figure 3). These findings were consistent with a clinical diagnosis of pityriasis lichenoides et varioliformis acuta (PLEVA).



Outcome of the case. Because PLEVA is considered to be self-limiting, and she strongly desired ongoing isotretinoin for her cystic acne, the decision was made to continue the patient on isotretinoin without discontinuation and rechallenge. Over the 5-month course of isotretinoin treatment, she experienced recurring papules to a lesser degree. A few varioliform scars presented in areas of crusting. There had been no further eruptions in the 2 months since she stopped isotretinoin.

Discussion. PLEVA is rare, and its incidence is not well documented; still, it is the most common subtype of pityriasis lichenoides, accounting for approximately 57% of cases.1 It occurs frequently in but is not isolated to the first 3 decades of life, and it occurs more commonly in men.2 Treatment for PLEVA is mostly supportive with close observation. It is possible for PLEVA to develop into a fatal form called febrile ulceronecrotic Mucha-Habermann disease. In general, time to remission varies from 1.6 to 18 months and appears to be affected by adult vs childhood onset of disease.1,3

Specific triggers in PLEVA have yet to be identified, but medications and infectious causes have been suggested.4 Correlations have been made between the similar histologic patterns of T-cell infiltration encountered in early lesions of PLEVA compared with the T-cell infiltration patterns of known drug antigens.5 Additionally, in one reported case of pityriasis lichenoides,6 T-cell monoclonality was seen in conjunction with genomic parvovirus B19 DNA, furthering conjecture about infection as a potential trigger. Further research is needed to elucidate if either or both are true underlying causes.

PLEVA does appear to be related to other lymphocytic eruptions given its monoclonal T-cell proliferation, suggesting that it may be a self-limiting form of T-cell dyscrasia. However, the affected cells in PLEVA demonstrate a CD8 cell preponderance not commonly seen in other T-cell dyscrasias. In addition, there is little evidence to suggest progression to other T-cell dyscrasias as is sometimes seen with pityriasis lichenoides chronica.7,8

Due to difficulty in identifying triggers, treatment options have been based on anecdotal and small case series. Oral antibiotics, topical corticosteroids, topical tacrolimus, and phototherapy have all been tried with varying success.9,10 Macrolides may be especially beneficial for their anti-inflammatory effects and the decrease in tumor necrosis factor α (TNF-α) that is increased in the febrile ulceronecrotic form of PLEVA.11,12 Erythromycin has successfully been used for treatment, which may be linked to its ability to inhibit T-cell proliferation and induce T-cell apoptosis—further enforcing the important role of cytotoxic T-cell response in PLEVA and its place as a T-cell dyscrasia.13 In the meantime, there may already be a role for TNF-α inhibitors in recalcitrant cases as shown by a reported case of improvement with etanercept for multidrug-resistant pityriasis lichenoides.14

Our review of the literature indicates no previous reports of isotretinoin exacerbating or inciting a PLEVA eruption. In our patient’s case, however, causality is difficult to prove due to the self-reported papules prior to isotretinoin initiation. Furthermore, tetracycline had been used for treating PLEVA in the past10 and may have been a factor in diminishing a preexisting PLEVA outbreak. However, the timing of the introduction to a potential trigger (ie, isotretinoin) and the patient’s corresponding increase in symptoms appear at least temporally related.

Interestingly, the degree of the patient’s skin involvement appeared to improve when isotretinoin was stopped after 6 months of treatment. The patient, however, was lost to follow-up 2 months after completing isotretinoin, leaving us uncertain about whether this improvement persisted or if it was a result of the self-limited course of the disease. This case is of interest because isotretinoin is often useful in treating inflammatory disorders such as acne or hidradenitis suppurativa. In our patient, however, there was a flare of symptoms similar to those rarely seen in initial phases of cystic acne treatment. 


  1. Ersoy-Evans S, Greco MF, Mancini AJ, Subaşi N, Paller AS. Pityriasis lichenoides in childhood: a retrospective review of 124 patients. J Am Acad Dermatol. 2007;56(2):205-210.
  2. Bowers S, Warshaw EM. Pityriasis lichenoides and its subtypes. J Am Acad Dermatol. 2006;55(4):557-572.
  3. Romaní J, Puig L, Fernández-Figueras MT, de Moragas JM. Pityriasis lichenoides in children: clinicopathologic review of 22 patients. Pediatr Dermatol. 1998;15(1):1-6.
  4. Khachemoune A, Blyumin ML. Pityriasis lichenoides: pathophysiology, classification, and treatment. Am J Clin Dermatol. 2007;8(1):29-36.
  5. Magro C, Crowson AN, Kovatich A, Burns F. Pityriasis lichenoides: a clonal T-cell lymphoproliferative disorder. Hum Pathol. 2002;33(8):788-795.
  6. Tomasini D, Tomasini CF, Cerri A, et al. Pityriasis lichenoides: a cytotoxic T-cell-mediated skin disorder. Evidence of human parvovirus B19 DNA in nine cases. J Cutan Pathol. 2004;31(8):531-538.
  7. Kempf W, Kazakov DV, Palmedo G, Fraitag S, Schaerer L, Kutzner H. Pityriasis lichenoides et varioliformis acuta with numerous CD30+ cells: a variant mimicking lymphomatoid papulosis and other cutaneous lymphomas. A clinicopathologic, immunohistochemical, and molecular biological study of 13 cases. Am J Surg Pathol. 2012;36(7):1021-1029.
  8. Vonderheid EC, Kadin ME, Gocke CD. Lymphomatoid papulosis followed by pityriasis lichenoides: a common pathogenesis? Am J Dermatopathol. 2011;​33(8):835-840.
  9. Wahie S, Hiscutt E, Natarajan S, Taylor A. Pityriasis lichenoides: the differences between children and adults. Br J Dermatol. 2007;157(5):941-945.
  10. Piamphongsant T. Tetracycline for the treatment of pityriasis lichenoides. Br J Dermatol. 1974;91(3):319-322.
  11. Alzolibani AA, Zedan K. Macrolides in chronic inflammatory skin disorders. Mediators Inflamm. 2012;2012:159354.
  12. Tsianakas A, Hoeger PH. Transition of pityriasis lichenoides et varioliformis acuta to febrile ulceronecrotic Mucha-Habermann disease is associated with elevated serum tumour necrosis factor-α. Br J Dermatol. 2005;152(4):794-799.
  13. Wu L, Zhang W, Tian L, Bao K, Li P, Lin J. Immunomodulatory effects of erythromycin and its derivatives on human T-lymphocyte in vitro. Immunopharmacol Immunotoxicol. 2007;29(3-4):587-596.
  14. Nikkels AF, Gillard P, Piérard GE. Etanercept in therapy multiresistant overlapping pityriasis lichenoides. J Drugs Dermatol. 2008;7(10):990-992.

NEXT: Minocycline-Induced Diffuse Pigmentation

Minocycline-Induced Diffuse Pigmentation

Cecelia Lau, MD; Ashley K. Bansal, MD; Erica K. Cichowski, MD; Freshta Sahak, MD; and Mahmoud Abu Hazeem, MBBS
Creighton University School of Medicine, Omaha, Nebraska


A 64-year-old man presented to his primary care physician for a yearly follow-up visit. His past medical history was significant for seborrheic dermatitis of the scalp and groin, rosacea, diffuse folliculitis, acne vulgaris, depression, benign prostate hyperplasia, and esophagitis. The patient had no significant social or family history and no known medication allergies.

Physical examination findings were remarkable for significant light blue ocular pigmentation of the conjunctiva (Figure 1), sublingual buccal mucosa (Figure 2), and gingival margins, with gray-blue pigmentation on the extensor surfaces of the legs (Figure 3), nails (Figure 4), and face. The rest of the physical examination findings, including cardiovascular, respiratory, and abdominal examination, were unremarkable. Laboratory test results, including a complete blood cell count, a comprehensive metabolic panel, a lipid panel, and thyrotropin/free thyroxine levels, were within normal limits.

Figure 1

Figure 2

Figure 3

Figure 4

The patient had been taking minocycline for approximately 15 years to control acne and rosacea. It was determined that the skin discoloration was secondary to extensive daily use of minocycline. Minocycline was discontinued, and he was started on benzoyl peroxide, 5%. 

One week after the medication change, the patient returned with concern for worsening acne. He wished to resume minocycline and was reluctant to try other medications. No improvement in the skin discoloration was noted during the 1 week.

Discussion. Minocycline is a broad-spectrum bacteriostatic antibiotic with a long half-life. There have been several documented cases of hyperpigmentation secondary to its use. Other adverse effects include diarrhea, vertigo, and autoimmune disorders. Minocycline-induced cutaneous pigmentation is categorized into 4 types (Table).1


Postinflammatory hyperpigmentation can also occur following any cutaneous injury or inflammation, especially in individuals with moderately or deeply pigmented skin.

Minocycline-induced hyperpigmentation of the skin and oral mucosa are generally reversible when the drug is discontinued. Pigmentation of all other sites can be permanent even after drug discontinuation. Treatment involves early recognition and discontinuation to prevent further pigmentation. Laser therapy and intense pulsed light can be used for persistent pigmentation.2

The bones of the oral cavity are the most frequently affected sites of pigmentation, with rates of greater than 20% for patients on minocycline therapy for more than 4 years. Uncommon sites of pigmentation include the oral mucous membranes and teeth, the ocular region, the thyroid, and visceral pigmentation.3 Long-term administration of minocycline at lifetime doses greater than 100 g results in general pigmentation. Cutaneous or oral mucosal pigmentation may appear regardless of the dose or duration of therapy. Sun exposure during therapy results in more frequent sunburns and increased likelihood of hyperpigmentation.

Generally, the drug is discontinued when adverse effects are seen, even though minocycline-induced pigmentation has not been shown to be harmful.

Our patient presented with types I and II hyperpigmentation. After discussing the risks and benefits of long-term minocycline usage, the patient wished to resume his regimen to control his acne and rosacea.


  1. Geria AN, Tajirian AL, Kihiczak G, Schwartz RA. Minocycline-induced skin pigmentation: an update. Acta Dermatovenerol Croat. 2009;17(2):123-126.
  2. Alster TS, Gupta SN. Minocycline-induced hyperpigmentation treated with a 755-nm Q-switched alexandrite laser. Dermatol Surg. 2004;30(9):1201-1204.
  3. Eisen D, Hakim MD. Minocycline-induced pigmentation: incidence, prevention and management. Drug Saf. 1998;18(6):431-440.

NEXT: Superscan Appearance on Radionuclide Bone Scan From Teriparatide

Superscan Appearance on Radionuclide Bone Scan From Teriparatide

Cathy Lee Ching, MD, and Suresh Kumar, MD
University of Miami Miller School of Medicine/JFK Medical Center Palm Beach Regional Campus, Atlantis, Florida


A 76-year-old man with rheumatoid arthritis, osteoporosis, and prostate cancer in remission, was started on subcutaneous teriparatide 20 µg daily for osteoporosis. One month later, a radionuclide bone scan that had been ordered for prostate cancer follow-up showed an “intense and diffuse tracer uptake throughout all the bones, with very faint renal uptake and minimal tracer within the urinary bladder, compatible with a superscan appearance” (Figure 1). No abnormal soft tissue uptake was seen.

This finding was concerning for diffuse metastatic prostate carcinoma; teriparatide was discontinued, and a repeat scan 1 month after stopping teriparatide showed that the superscan appearance had resolved, with increased uptake seen only in both knees, likely representing degenerative changes (Figure 2).

This case illustrates that teriparatide can cause changes in radionuclide scans, mimicking cancer, myelofibrosis, or hyperparathyroidism, and that these changes can resolve as early as 1 month after stopping the medication.

Teriparatide treatment should be in the differential diagnosis of a superscan appearance on a bone scintigraphy image.