Case Presentation: A 64-year-old woman with benign paroxysmal positional vertigo (BPPV), anxiety, muscle spasticity, and frequent falls presented to the emergency department with acute right hip pain. She normally ambulated with a walker due to bilateral stiffness and intermittent leg pain. Two years earlier, neurology noted increased tone, spasticity, and a wide-based, slow gait with difficulty initiating. Head CT showed minimal small-vessel ischemic changes, and she was started on meclizine for BPPV.She was in her usual state of health until her son attempted to lift her from bed, triggering sudden, non-radiating right hip pain. ED imaging confirmed a right femoral neck fracture, and she underwent urgent fixation with a cephalomedullary nail.On postoperative day (POD) 1 she developed bilateral lower-extremity rigidity, left leg pain, and inability to move the right leg. Passive ROM was not tolerated (worse on the left). She had moderate–severe rigidity of the upper extremities and areflexia throughout. CK was 5259 and creatinine 1.4, consistent with postoperative rhabdomyolysis. Brain and spine MRI were unrevealing. EMG demonstrated myopathy and distal axonal polyneuropathy, explaining weakness but not rigidity. CSF showed elevated protein without infection or inflammation. On POD 6, CSF GAD65 antibody was positive at 16.9, consistent with stiff person syndrome (SPS). Her stiffness and pain improved with gabapentin, baclofen, and benzodiazepines, and she was discharged to subacute rehabilitation with gradual improvement.

Discussion: Stiff person syndrome spectrum disorders (SPSSD) are rare autoimmune neurologic disorders affecting an estimated 1–2 per million, most commonly women ages 20-50 [1]. This report is one of two published cases describing SPSSD diagnosis after trauma [2]. Classic SPS presents with asymmetric, progressive trunk and limb rigidity with painful spasms triggered by sudden environmental or emotional stimuli; gait impairment and anxiety disorders may also occur, complicating diagnosis [3,4]. Conditions that mimic SPSSD include Parkinson’s disease, atypical parkinsonian syndromes, multiple sclerosis, and functional neurologic disorders. Anti–glutamic acid decarboxylase (GAD) antibodies are implicated in reduced GABA synthesis and subsequent neuronal hyperexcitability [5]. Though not universally present, high GAD65 titers are highly specific for SPSSD, and continuous motor unit activity on EMG supports the diagnosis [6]. First-line therapy is high-dose benzodiazepines and baclofen, with adjunctive GABAergic agents; IVIG is used for severe or refractory symptoms [7]. SSPDs should be thought of for any patient who has undergone work up for asymmetric muscle stiffness and pain with sudden spasms that does not find conclusive evidence on MRI.

Conclusions: SPSSD are likely underdiagnosed due to nonspecific early symptoms and variable presentations. This case highlights the need to consider SPSSD in patients with unexplained asymmetric stiffness, painful spasms, and negative MRI findings, especially in the post-traumatic setting.