Anterior spinal cord syndrome as a rare complication of acute bacterial meningitis in an adult

Abstract

Acute bacterial meningitis is not an uncommon central nervous system infection. In severe cases, it can be associated with various neurological or systemic complications. However, acute spinal cord dysfunction rarely occurs. We report a case of bacterial meningitis complicated with spinal cord infarction despite adequate treatment with antibiotics and corticosteroid therapy. He had residual paraplegia and was fully dependent in the activity of daily living.

Background

Brain complications have been widely described in bacterial meningitis. These include seizure, stroke, hydrocephalus, hearing loss, subdural empyema, brain abscess, cranial neuropathy, venous sinus thrombosis, cognitive impairment and hypothalamic–pituitary dysfunction.¹ Complications involving the spinal cord are very rare and their occurrence in the literature is based only on case reports. However, these can develop at any time despite treatment in a susceptible patient. Recognition of the predisposing factors and early prevention may help to reduce the risk of devastating neurological dysfunction.

Case presentation

A 28-year-old, previously healthy man was admitted to local hospital with fever and abdominal pain since 4 days prior, associated with headache and vomiting. He was diagnosed with acute appendicitis, received antibiotics and subsequently underwent appendicectomy. The intraoperative finding was mildly inflamed appendix.

However, 24 hours after the surgery, he became delirious. There was no history of seizure, abnormal behaviour, memory or cognitive impairment during the course of illness. There was no back pain, joint pain, rashes or other symptoms to suggest connective tissue diseases. He never consumed illegal drugs or alcohol. There was no high-risk behaviour to suggest immunocompromised state. Review of other systems was normal. Subsequently, he was transferred to our hospital for further management.

On arrival to emergency room, he was drowsy and confused. He had fever with temperature of 39.6°C. Other vital signs were unremarkable. Neurological examination revealed significant nuchal rigidity with positive Kernig’s and Brudzinski’s signs. He was able to move all extremities equally with normal deep tendon reflexes and flexor plantar response. The appendicectomy scar appeared clean without any discharge. Other system examinations were normal.

Investigations

Laboratory tests showed leucocytosis. Erythrocyte sedimentation rate and C-reactive protein were raised. Contrast-enhanced brain CT disclosed nothing abnormal. Lumbar puncture was performed and the opening pressure was raised to 33 cmH₂O. Cerebrospinal fluid (CSF) examination revealed clear fluid with lymphocyte count of 50 x 10⁹/L, red blood cell count of 0.82 x 10¹²/L/, raised protein 1.72 g/L and low glucose level of 2.4 mmol/L (CSF:serum ratio <40%). Unremarkable results were obtained from CSF gram stain, culture, polymerase chain reaction (PCR) for herpes simplex virus 1 and 2, acid-fast bacilli staining and PCR for Mycobacterium tuberculosis, India ink test, cryptococcal antigen and latex agglutination test for common bacteria. Results of other tests for human immunodeficiency virus (HIV), venereal disease research laboratory (VDRL), connective tissue disease, chest X-ray and tuberculin test were normal. Screening for Listeria monocytogenes was not performed due to unavailability of the test.

Differential diagnosis

Differential diagnosis includes acute bacterial meningitis, intra-abdominal sepsis with encephalopathy and subarachnoid haemorrhage due to vasculitis.

Treatment

He was monitored in intensive care unit. Intravenous ceftriaxone and metronidazole was prescribed, together with intravenous dexamethasone. He had an episode of non-convulsive seizure, and antiepileptic drug levetiracetam was instituted.

His blood pressure became hypotensive and he had persistent fever even after 48 hours of admission, thus the antibiotic was switched to intravenous meropenem in view of ongoing sepsis. He was intubated and required vasopressor therapy to stabilise his blood pressure. Echocardiogram result was normal. The CSF examination was repeated after 72 hours of meropenem, which showed improvement with absence of cells, normalisation of glucose and reduction of protein level. The antibiotic was continued.

After 2 weeks of mechanical ventilation and completion of antibiotic, he regained full conscious state and was extubated. However, he was noted to be paraplegic. Examination revealed bilateral lower limb strength of Medical Research Council (MRC) grade 0/5 and normal upper extremities. There was absence of sensation to pinprick, temperature and soft touch from T9 dermatome and distally, but with preserved proprioception and vibration sense. He also had bladder and bowel dysfunction.

Diagnosis of anterior spinal cord syndrome was made. Spine MRI was performed and showed spinal dural enhancement from T7–L1 spine (figure 1 and figure 2), but more diffuse and prominent distally. The cord was abnormal with predominantly central intramedullary hyperintensity on Short-Tau Inversion Recovery (STIR) and T2-weighted MRI (figure 3). There was no cord enhancement post contrast or abscess formation. The nerve conduction study result was normal.

Figure 1.

T1-weighted spine MR, postcontrast image shows spinal dural enhancement, which is more prominent distally. No intramedullary enhancement seen.

Figure 2.

Axial T1-weighted spine MR, postcontrast image shows dural enhancement surrounding the spinal cord.

Figure 3.

Patchy intramedullary cord hyperintensity on T2 Short-Tau Inversion Recovery (T2-STIR) MRI.

Outcome and follow-up

He underwent rehabilitation and physiotherapy. Despite normal cognitive function, the spinal cord complication was persistent with residual paraplegia and bladder dysfunction. At follow-up visits, his lower limb weakness remained similar.

Discussion

Diagnosis of bacterial meningitis in our patient was based on acute history of fever, headache, drowsiness and presence of signs of meningeal irritation.¹ The initial CSF examination showed features of partially treated bacterial infection. Prior antibiotic usage may explain the negative CSF culture and predominant lymphocytes rather than polymorphs.¹ In addition, the repeated CSF examination confirmed improvement of disease with antibiotic therapy.

During the clinical course of bacterial meningitis, focal neurological deficits were found in 50% of adult patients.² Spinal cord dysfunction may rarely occur due to various mechanisms, such as cord compression secondary to spinal or epidural abscess and haematoma following lumbar puncture. It can also be affected as a result of non-compressive lesions such as hypoperfusion in shock leading to cord ischaemia or infarction, vasculitis, arachnoiditis, direct infection or secondary immune-mediated myelitis and polyradiculitis.³

Our patient presented with typical features of anterior cord syndrome. This includes sensory level with impaired pain and temperature below the level of the lesion. The dorsal column function of proprioception and vibration are spared. Weakness occurs due to disruption of descending corticospinal tracts. Involvement of ventral grey matter may manifest as lower motor neuron type of weakness.⁴ Other symptoms vary such as autonomic dysfunction, bladder or bowel disturbance.⁵

Acute anterior cord syndrome is commonly due to anterior spinal artery (ASA) ischaemia or infarction. The onset of symptoms is commonly abrupt as a result of sudden impairment of arterial flow. ASA is the major arterial supply to the anterior two-thirds of the spinal cord. It originates from the branches of vertebral artery. This area is more susceptible to ischaemia because the branches are end arteries and have no anastomoses.^{4 6} Anterior spinal artery infarction may also occur due to impairment of perfusion via the great anterior radicular artery of Adamkiewicz, which is the major contributor to the caudal two-thirds of ASA in the region of lower thoracic and lumbar (T5 to L2) segment of the spinal cord.⁴ Other major causes of disruption of blood flow in ASA are occlusion due to emboli or atheroma, aortic dissection, aneurysm, trauma or syphilitic arteries.⁴ However, these causes are less likely to occur in our patients, as he did not have any risk factors.

Several mechanisms contributed to spinal cord infarction or ischaemia in bacterial meningitis. Occurrence of systemic hypotension, as seen in our case, is a known precipitating factor, resulting in impaired perfusion to the spinal cord and subsequent development of infarction.⁷ Arachnoiditis is the second possible mechanism. In our patient, MRI showed evidence of meningeal enhancement at the distal thoracic and lumbar cord region which supports the presence of meningeal inflammation. Infection and inflammatory changes in the subarachnoid space can lead to progressive arachnoid adhesion which compromise the blood flow in small arteries supplying the spinal cord. It also causes venous congestion and ischaemia.⁸ De Schryver et al reported a case of extensive spinal cord dysfunction following Staphylococcus aureus septicaemia in meningitis, with the postulated mechanism that was likely due to disruption of the blood supply secondary to extensive arachnoiditis.⁹ Spread of purulent infection or inflammation surrounding the blood vessels could also cause septic venous thrombosis and vasculitis of spinal arteries which lead to ischaemia.¹⁰ Boothman et al reported a case of meningococcal meningitis with paraplegia due to intramedullary vasculitis.¹¹ Most of these mechanisms occur early in the course of illness when the infection is still active. Common pathogens that were associated with spinal cord dysfunction in adult meningitis include Neisseria meningitidis, Streptococcus pneumoniae and Haemophilus influenzae.^{3 8}

Apart from spinal cord infarction, the anterior portion of the cord may also be affected by a form of myelitis either due to direct infection or secondary immune-mediated inflammation. Nevertheless, during postmortem examination in purulent meningitis, myelitis has been rarely demonstrated.³ In adults, myelitis secondary to meningitis has a predilection for the mid-thoracic and lumbar region.¹² Postinfectious immune-mediated myelitis usually occurs during the resolution phase of infection, between the first and third week of illness.

MRI finding of multiple spinal cord segment hyperintensities on T2-weighted image is seen in both myelitis and infarction. In acute stage, the presence of cord oedema and contrast enhancement aids in discriminating it from infarction. These findings are supportive but not specific to any type of myelitis. During the subacute phase of disease, both myelitis and infarction may show cord enhancement post contrast.¹³ In this patient, the radiological features of very minimal spinal cord oedema and without intramedullary contrast enhancement are more supportive of vascular compromise rather than myelitis. Predominant central cord involvement, as observed in our patient, indicates venous congestion.³

Despite the lack of pathological confirmation, and various mechanisms that may coexist, we postulated that the anterior cord syndrome in our patient is most likely due to infarction, primarily based on the available clinical and radiological evidences.

Learning points.

• Bacterial meningitis can lead to severe systemic and neurological complications.

• Spinal cord infarction (SCI) is rarely encountered but may result in severe debilitating neurological deficit.

• Multiple mechanisms predispose to SCI in bacterial meningitis, such as hypoperfusion, arachnoiditis, vasculitis and venous congestion.

• This complication may occur at any time despite adequate antibiotic and steroid therapy.

• Prevention of hypoperfusion may help to reduce risk of SCI in bacterial meningitis.