Paralysis in an adult man: quadriparesis/paraparesis.

A 23 year old laborer needs to be evaluated. He has been in bed for almost 3 months because his limbs are paralysed to the extent that he needs to be lifted up into a wheelchair and also when he needs a bath or a change of apparel. He needs a urinary catheter but can pass stool after being given an enema or a suppository. He has had no trauma to the neck, shoulder or head. The illness developed over 3-4 days without any headache or pain in the neck or fever. He became totally paralysed from below upwards and is now appearing to get better. On examination you find that all four limbs are involved, with marked hypertonia, grade 2-3 muscle weakness and 4-5 increased motor reflexes and up-going planter reflexes. There is no significant sensory loss. Because of the marked weakness ataxia is difficult to assess.

What is this condition?

In a regional neuroscience center in the United Kingdom, the most common cause of spastic paraparesis or quadriparesis among 585 patients was cervical spondylotic myelopathy (24 percent), followed by tumor (16 percent), multiple sclerosis (MS; 18 percent), and motor neuron disease (4 percent)

Is this transverse myelitis?

TM is a segmental spinal cord injury caused by acute inflammation usually idiopathic in origin which results in paraplegia, quadriplegia, or the Brown-Sequard syndrome. It is rapid in onset and upper motor neuron in origin. It usually occurs over a few segments and the sensory loss may be missed.TM can also occur in multiple sclerosis (MS) and can be the presenting demyelinating event. Neuromyelitis optica or Devic disease is a disorder related to MS. Remember to examine the fundi and give the reason for doing so. Connective tissue disorders can also cause TM such as systemic lupus erythematosus, mixed connective tissue disease, Sjögren’s syndrome, scleroderma, antiphospholipid antibody syndrome, ankylosing spondylitis, rheumatoid arthritis. 

Magnetic resonance imaging (MRI) of the involved section of the spinal cord shows gadolinium-enhancing signal abnormality, usually extending over one or more cord segments. The cord often appears swollen at these levels. Cerebrospinal fluid (CSF) is abnormal in half of patients, with elevated protein level (usually 100 to 120 mg/100 mL) and moderate lymphocytosis (usually <100/mm3). Glucose levels are normal. Oligoclonal bands are usually not present in isolated TM, and when present suggest a higher risk of subsequent MS

The granulomatous inflammation of sarcoidosis can affect the spinal cord and produce an acute or subacute segmental myelopathy. The lesions can be extramedullary or intramedullary, and can involve the cauda equina as well as the cord. MRI signal abnormalities are not specific; neurosarcoid lesions can appear similar to TM or can resemble a tumor. CSF evaluation usually shows elevated protein and/or pleocytosis. Hilar lymphadenopathy may suggest the diagnosis; however, serum and CSF angiotensin converting enzyme levels are neither sensitive nor specific for neurosarcoidosis. Patients with neurologic sarcoidosis are generally treated with corticosteroids and other immunomodulatory agents and can improve.

Paraneoplastic syndromes. Four of these occur are likely to be seen but are unlikely to be present in this patient. These are given below:

  • Motor neuron syndrome – a subacute, progressive, painless, and often asymmetric lower motor neuron weakness, most often associated with lymphoma
  • Acute necrotizing myelopathy – a rapidly ascending syndrome of sensory deficits, sphincter dysfunction, and flaccid or spastic paraplegia or quadriplegia
  • Subacute sensory neuronopathy – an inflammatory disorder affecting the dorsal root ganglia, producing progressive loss of sensory modalities, leading to prominent ataxia. This is most often associated with small cell lung cancer and anti-Hu antibodies.
  • Encephalomyelitis – a diffuse involvement of brain and spinal cord regions, in which cerebral manifestations frequently overshadow the myelopathy. Several syndromes are described.

Is it an acute infection?

Tuberculosis — Tuberculosis can produce a myelopathy by different mechanisms. Infection of the vertebral body leads to tuberculous spondylitis or Pott’s disease, which can lead to secondary cord compression. These patients present with back pain over the affected vertebra, low-grade fever, and weight loss, followed by a secondary compressive myelopathy. Tuberculomas within the intramedullary, intradural, and extradural space can also produce myelopathy.

Think of an acute epidural abscess specially one caused by Staph. It is a reversible cause of the paralysis. The infection can originate via contiguous spread from infections of skin and soft tissues or as a complication of spinal surgery and other invasive procedures, including indwelling epidural catheters. Other cases of epidural abscess arise from a remote site via the bloodstream. Diabetes, alcoholism, and human immunodeficiency virus (HIV) infection are risk factors.

Acute viral myelitis — Two distinct syndromes of spinal cord involvement are associated with acute viral disease. In the first, the virus targets the gray matter of the spinal cord, producing acute lower motor neuron disease. These viruses include:

●Enteroviruses, such as poliovirus, coxsackie virus, and enterovirus 71.

●Flaviviruses, such as West Nile virus and Japanese encephalitis virus.

AIDS myelopathy — HIV infection produces a vacuolar myelopathy, which is found in up to half of patients with AIDS at autopsy. However, clinical manifestations occur when the pathology is advanced, and only approximately one-fourth of patients demonstrating vacuolar myelopathy at autopsy have symptoms during life.

HTLV-I myelopathy — Human T-lymphotropic virus type I (HTLV-I) causes a progressive neurologic disease, which is called either HTLV-1-associated myelopathy (HAM) or tropical spastic paraparesis (TSP) [57,58]. This disorder is endemic in southern Japan, the Caribbean, South America, the Melanesian islands, Papua New Guinea, the Middle East, and central and southern Africa, with sero prevalence as high as 30 percent in southern Japan.

Spinal cord infarction is most frequently caused by surgical procedures and pathologies affecting the aorta but can also occur in the setting of severe systemic hypotension or cardiac arrest. Symptoms are consistent with the functional loss within the anterior spinal artery territory and include paralysis, loss of bladder function, and loss of pain and temperature sensation below the level of the lesion. Position and vibratory sensation are spared. The onset of symptoms is sudden and is frequently associated with back pain. Magnetic resonance imaging (MRI) will demonstrate a T2 signal change consistent with cord ischemia, but may be normal in the first 24 hours.

Think also of spinal a-v malformations and hematomas.

Subacute combined degeneration — Deficiency in vitamin B12 (cobalamin) leads to degeneration of the dorsal and lateral white matter of the spinal cord, producing a slowly progressive weakness, sensory ataxia, and paresthesias, and ultimately spasticity, paraplegia, and incontinence. Not all patients with neurologic abnormalities will have anemia or macrocytosis. Supplemental treatment with vitamin B12 can stop progression and will produce neurologic improvement in most patients.

Two causes of spinal cord degeneration are linked to food and are found in times of famine. Neurolathyrism is associated with prolonged consumption of the grass or chickling pea (Lathyrus sativus). Exposed persons develop a slowly developing spastic paraparesis with cramps, paresthesias, and numbness, accompanied by bladder symptoms and impotence. Konzo, a disorder characterized by acute spastic paraparesis or quadriparesis, is linked to high exposure to cyanogenic compounds in diets containing insufficiently processed bitter cassava (Manihot esculenta).

Both benign and malignant tumors can produce a myelopathy as a result of external compression or intramedullary growth.

Neoplasm. The most common syndrome is that of extradural spinal cord compression, as produced by metastases to the extradural space. Patients present with a progressive weakness below the level of the lesion with accompanying sensory loss and bladder dysfunction. Diagnostic evaluation (with gadolinium-enhanced spinal magnetic resonance imaging [MRI]) must proceed promptly when this diagnosis is considered. Intramedullary spinal cord tumors are typically primary central nervous system tumors (ependymoma, astrocytoma); metastases are less likely. These produce a progressive myelopathy, often with central cord features. MRI with gadolinium will show the tumor. Myelopathy can also occur as a complication of radiation therapy.

Is this Friedreich’s ataxia?

The neuropathologic changes in Friedreich ataxia include degeneration of the posterior columns and the spinocerebellar tracts of the spinal cord and loss of the larger sensory cells of the dorsal root ganglia. These findings correspond to the clinical manifestations of progressive ataxia of all four limbs and gait, weakness, absent reflexes with extensor plantar responses, loss of position and vibration sense, and sparing of pain and temperature. Cardiomyopathy and diabetes mellitus are part of the syndrome. Patients with late-onset disease are more likely to have retained reflexes, spasticity, and no cardiomyopathy. MRI may show atrophy of the cervical cord. Disease severity and rate of progression are highly variable. This condition is unlikely in this patient as he came in with muscle weakness not ataxia, he has no dysphasia, dysphagia, loss of sense of position and vibration. His reflexes are exaggerated and muscle tone increased. In Friedreich’s ataxia in very late onset cases there may rarely be spasticity. Check out genetic evidence of frataxin repeats (GAA), frataxin level, vitamin E level in serum (should be normal) and no cerebellar atrophy on the MRI of the brain. There is no cure.

This is an extensive subject. I have not touched on traumatic myelopathy but i have given you plenty of thought for reading up for an exam and answering some of the common questions likely to be asked.

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I am a Professor of Medicine and a Nephrologist. Having served in the Army Medical College, Pakistan Army for 27 years I eventually became the Dean and Principal of the Bahria University Medical and Dental College Karachi from where I retired in 2016. My passion is teaching and mentoring young doctors. I am associated with the College of Physicians and Surgeons Pakistan as a Fellow and an examiner. I find that many young doctors make mistakes because they do not understand how they should answer questions; basically they do not understand why a question is being asked. My aim is to help them process the information they acquire as part of their education to answer questions, pass examinations and to best take care of patients without supervision of a consultant. Read my blog, interact and ask questions so that I can help you more.

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