Presentation of Case

A 72-year-old right-handed man was admitted to the hospital because of neck pain and weakness of both shoulders after generalized tonic–clonic seizures.

The patient had previously been healthy and independent. Two years earlier, he had been diagnosed with transient global amnesia and had subsequently been treated with carbamazepine, although medication adherence was poor. In September 2022, while asleep at home, he developed a witnessed generalized tonic–clonic convulsion. There was no reported fall or direct trauma.

He was brought to the emergency department by family members while unconscious. A computed tomographic (CT) scan of the brain was obtained and showed no acute abnormalities; the cranio-cervical junction was interpreted as normal.

During the next 24 hours, two additional generalized tonic–clonic seizures occurred. Seizures were controlled with intravenous levetiracetam.

After the postictal period resolved, the patient complained of severe neck pain and stiffness. He was unable to raise either arm above shoulder level. Despite these symptoms, he remained ambulatory and denied sensory loss, respiratory symptoms, bowel dysfunction, or bladder dysfunction. Examination revealed no cranial nerve abnormalities, reflex asymmetry, or lower-extremity weakness.

Radiographs of both shoulders excluded dislocation. Stroke was considered unlikely because the weakness was symmetric and unaccompanied by cranial nerve or lower-extremity findings. Since the CT scan had reportedly demonstrated a normal cranio-cervical junction, the symptoms were attributed to postconvulsive muscle spasm and cervical spondylosis. Conservative management with analgesics and physiotherapy was initiated.

Over the course of a month, the shoulder weakness and pain gradually improved, although neck stiffness persisted.

One year later, because of persistent neck symptoms, magnetic resonance imaging (MRI) of the cervical spine was obtained. Imaging revealed a type II odontoid fracture with fracture separation and associated retrodental soft-tissue thickening.

What is the differential diagnosis?

Differential Diagnosis

This patient presented with painful bilateral shoulder weakness after generalized seizures. The immediate diagnostic challenge is determining whether the symptoms reflect:

• a musculoskeletal complication of seizure activity,
• a peripheral neurologic injury,
• or occult cervical spinal cord pathology.

Postictal muscle pain is common after generalized tonic–clonic seizures and initially appears plausible. Violent tonic contractions may produce muscular strain, shoulder pain, or transient weakness. Shoulder dislocation and proximal humeral fractures must also be considered, although radiographs were negative in this patient.

Bilateral arm weakness after seizures also raises concern for:

• cervical radiculopathy,
• brachial plexopathy,
• spinal epidural hematoma,
• cervical disc herniation,
• ischemic stroke,
• or cervical spinal cord injury.

The key clinical features in this case are:

• severe neck pain,
• restricted cervical motion,
• bilateral arm weakness,
• relative sparing of the legs,
• and the temporal relationship to repeated generalized convulsions.

These findings strongly suggest cervical spinal pathology.

The question then becomes:

Could a seizure alone produce an unstable cervical fracture in the absence of direct trauma?

The answer is yes.

Diagnostic Reasoning

Spinal fractures following seizures are uncommon but well recognized. Most seizure-induced fractures involve the thoracic or lumbar spine. Odontoid fractures are particularly rare.

The odontoid process serves as the principal fulcrum for cervical rotation and stability. Type II odontoid fractures occur at the junction between the odontoid base and the body of C2 and are considered unstable injuries.

Several diagnostic clues were present early in this patient’s course:

• disproportionate neck pain,
• painful restriction of movement,
• inability to raise both arms,
• persistence of symptoms beyond the immediate postictal period.

However, the diagnosis was obscured by two cognitive errors.

First, clinicians anchored on a common explanation: postictal muscle spasm superimposed on cervical spondylosis.

Second, there was overreliance on an initially negative CT interpretation of the cranio-cervical junction.

The gradual improvement in arm pain and weakness likely reflected recovery from transient neuropraxia and partial cord irritation rather than resolution of the underlying instability.

The persistent neck stiffness was a critical clue. The authors propose that posterior cervical musculature may have functioned as a compensatory stabilizing mechanism to prevent atlantoaxial subluxation.

One year later, MRI revealed the true diagnosis:

Evolution of Neurologic Symptoms

Despite conservative treatment, the patient later developed:

• impaired fine motor function,
• hand clumsiness,
• difficulty buttoning his shirt,
• difficulty feeding himself,
• impaired pain and temperature sensation in the hands,
• and gait instability.

Remarkably, proprioception and bowel and bladder function remained preserved.

MRI demonstrated narrowing of the upper cervical spinal canal with cord compression and T2/STIR hyperintensity within the cervical cord, findings consistent with early compressive myelopathy.

The pattern of deficits suggested:

Central cord syndrome.

Neuroanatomic Correlation

Central cord syndrome is the most common incomplete cervical spinal cord injury. It classically produces:

• disproportionately greater weakness in the arms than in the legs,
• impaired hand dexterity,
• variable sensory loss,
• relative sparing of lower-extremity function.

The neuroanatomic explanation is illustrated elegantly in the schematic diagram on page 4 of the report, which demonstrates preferential involvement of centrally located corticospinal fibers subserving upper-extremity function and spinothalamic decussating fibers mediating pain and temperature sensation.

The patient’s dissociated sensory loss — impaired pain and temperature sensation with preserved proprioception — further localized the lesion to the central cervical cord.

Discussion

This case illustrates several important principles in neurologic diagnosis.

First, generalized tonic–clonic seizures may produce significant skeletal injuries even in the absence of external trauma. Violent muscular contractions alone can generate sufficient biomechanical force to produce cervical instability.

Second, persistent or disproportionate neck pain after seizures should never be dismissed casually. A normal initial study does not exclude evolving cervical pathology, particularly in older adults with degenerative cervical disease.

Third, the neurologic examination evolved over time. Initially, the patient demonstrated pain-limited weakness without overt myelopathy. Only later did the characteristic findings of central cord syndrome emerge:

• hand dysfunction,
• cape-like dissociated sensory deficits,
• gait disturbance,
• relative sparing of bowel and bladder function.

Fourth, delayed recognition likely contributed to nonunion and progressive instability. The authors emphasize that early cervical immobilization following suspicious postictal neck symptoms may prevent devastating neurologic complications.

The MRI and CT images shown on page 5 demonstrate fracture separation of the odontoid process with anterior compression of the cervical spinal cord and intramedullary T2 signal abnormality consistent with compressive myelopathy.

Ultimately, because of progressive neurologic decline and radiographic evidence of cord compression, the patient underwent cranio-cervical fixation. Within two weeks, substantial improvement in hand dexterity and gait occurred.

Clinical Diagnosis

Type II odontoid fracture following generalized tonic–clonic seizures, resulting in delayed central cord syndrome due to cervical cord compression.

Teaching Points

• Severe neck pain after a generalized seizure should prompt evaluation for cervical spinal injury.
• Seizure-induced odontoid fractures may occur without direct trauma.
• Persistent neck stiffness is an important warning sign of occult cervical instability.
• Central cord syndrome classically causes arm weakness greater than leg weakness with impaired hand dexterity.
• Dissociated sensory loss with impaired pain and temperature sensation localizes to centrally located spinothalamic fibers.
• Initial imaging may fail to reveal unstable cervical injury.
• Early cervical immobilization and spinal evaluation are critical in suspicious postictal presentations.

Clinical Take-Home Message

Generalized tonic–clonic seizures can produce unstable cervical fractures even in the absence of overt trauma. In patients with severe postictal neck pain, restricted neck motion, or bilateral arm weakness, occult cervical spinal injury must be considered immediately. Delayed diagnosis of odontoid fracture may result in progressive cervical cord compression and central cord syndrome, whereas timely recognition and stabilization may prevent irreversible neurologic disability.