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Hyporeflexia is the condition of below normal or absent reflexes (areflexia). It can be tested for by using a reflex hammer. It is the opposite of a condition called hyperreflexia.[1]

Hyporeflexia is generally associated with a lower motor neuron deficit (at the alpha motor neurons from the spinal cord to muscle), whereas hyperreflexia is often attributed to upper motor neuron lesions (along the long motor tracts from the brain). The upper motor neurons are thought to be inhibitory of the reflex arc, which is formed by sensory neurons from intrafusal fibers of muscles, lower motor neurons (including alpha and gamma motor fibers) and appurtenant interneurons. Therefore, damage to lower motor neurons will subsequently lead to hyporeflexia and/or areflexia.[2]

Note that in spinal shock, which is commonly seen in transection of the spinal cord (Spinal cord injury), areflexia can occur transiently below the level of the lesion and after a period of time become hyperreflexic.


Hyporeflexia is a reduced or absence of reflex in response to a stimulus, like contact with a reflex hammer or medical instrument. It is a sign of a neurological problem, indicating that something is wrong with a patient’s sensory or motor neurons in the area of interest. This may be uncovered during a routine neurological evaluation or as part of testing to determine the extent and origins of a known medical problem. Treatment options can depend on why the patient’s reflexes are impaired.[3] Deep tendon reflexes are routinely tested on neurologic exam, and although nonspecific, can help in localizing neurologic lesions. They can be decreased by any process that affects the reflex arc (lower motor neuron, muscle, sensory neuron), by acute upper motor neuron lesions, and by mechanical factors (e.g., joint disease). Hyporeflexia is usually a general indicator of lower motor neuron dysfunction, which may result from a lesion anywhere in the anterior horn cell, spinal motor nerve or nerve root plexus, peripheral nerve, neuromuscular junction, or muscle. Hyporeflexia alone, in the absence of pathology, generally causes no disability and requires no treatment. Reflexes are graded as (0) no reflex, (1), reflex with reinforcement procedures, (2), normal reflex, (3), brisk reflex with spread to other muscles, (4) sustained clonus.[4]


Hyporeflexia is most commonly caused by:

  • Peripheral neuropathy
  • Radiculopathy
  • Guillain–Barré syndrome
  • Disorders of the anterior horn cells
  • Hyperacute upper motor neuron injury
  • Normal variant [5]


History and physical examination:

  • Assess present illness, time course of symptoms (acute vs. chronic), past history, family history of neurologic diseases, and medications.
  • Perform a complete neurologic history and exam, and note other associate neurologic findings and definicits (e.g., weakness, sensory level, Babinski's sign).
  • Musculoskeletal exam for muscle bulk, consistency, tenderness, and tone.
  • Assess deep tendon reflexes while limbs are in relaxed and symmetric position; if a reflex cannot be elicited, use reinforcement procedures (grit teeth, press hands together).
  • Etiologic (e.g., neuropathy or myopathy) may be specified by associated signs on physical exam (e.g., symmetric stocking-glove territory sensory loss in association with hyporeflexia suggests peripheral neuropathy; isolated loss in association weakness of ankle plantar flexion suggests S1 radiculopathy)
  • Lower motor neuron lesions are associated with weakness, muscle atrophy, fasciculations (visible contractions), and hypotonia, in addition to hyporeflexia; upper motor neuron lesions are associated with weakness, hyperreflexia, hypertonia, and extensor plantar responses.

Initial diagnostic workup

  • Nerve conduction studies and EMG are useful in evaluating suspected peripheral polyneuropathy, single or multiple mononeuropathies, radiculopathy, or myopathy
  • MRI of the spine may help to diagnose radiculopahty
  • Consider muscle and/or nerve biopsy
  • If suspect Guillain-Barre syndrome or chronic inflammatory demyelinating polyneuropathy, CSF analysis may show elevated protein levels; reflexes will be diffusely absent or absent in lower extremities first.
  • For generalized peripheral neuropathy, further labs include CBC, electrolytes, glucose, calcium, SPEP, UPEP, ESR, ANA, RF, HIV, RPR, vitamin B12, creatine phosphokinase, thyroid function tests, HbA1c, and heavy metal screen.
  • Consider cardiac evaluation (cardiomyopathy may coexist)

Initial patient management

  • Hyporeflexia alone is not an indication for treamtnet; no disability may be associated with hyporeflexia, but treatment varies depending on underlying cause
  • Weakness and hypotonia may require physical therapy and bracing
  • Treat identified causes of peripheral neuropathy (e.g., thyroid diaseas, vitamin B12 deficientcy)
  • Guillain Barre syndrome has improved outcome if treated with plasmapherisis or IVIG within 2 weeks of the onset of the symptoms
  • Radioculopathy may be treated conservatively with physical therapy and medications (e.g., NSAIDs), more aggressively with epidural steroid injections, or surgically
  • Other cases of focal hyporeflexia (e.g. traumatic nerve injury) are treated individually, but usually the only option is supportive care while awaiting spontaneous recovery or surgery

Differential Diagnosis:

Peripheral Neuropathy:

  • Most common cause of symmetric hyporeflexia (polyneuropathy or mononeuropathy)
  • May present with symmetric sensory complaints or weakness with distal muscular atrophy
  • Most frequently associated with diabetes, other etiologies including hypothyroidism, syphilis, vitamin B12 deficiency, CIDP, and others

Isolated peripheral nerve injury/dysfunction

  • Trauma
  • Postsurgical
  • Tumor compression


  • Isolated loss of a single reflex may suggest dysfunction of that nerve root (ankle reflex, S1, 2, nerve root; knee jerk, L3, 4; biceps, C5, 6; triceps C7, 8)
  • Associated symptoms may include dermotomal sensory loss or pain and weakness of muscles in the territory of the affected root

Guillain Barre syndrome

  • Results from inflammatory demyelination (likely viral) or peripheral nerves
  • Produces subacute onset of progressive weakness (hours to days) and hypot-or areflexia
  • Patients may experience respiratory compromise or autonomic dysfunction

Brachial or lumbosacral plexopathy

  • May be spontaneous or secondary to trauma
  • Usually associated with severe pain in shoulder and arm (brachial plexopathy) or hip and leg (lumbosacral plexopathy)

Lambert-Eaton myasthenic syndrome

  • Presynaptic neuromuscular disease associated with small cell carcinoma of the lung multifocal motor neuropathy
  • May mimic amyotrophic laterial sclerosis but without upper motor neuron signs


  • Patients present primarily with weakness but may also exhibit hyporeflexia
  • Muscular dystrophy
  • Myotonic dystrophy

Motor Neuron Disease

  • Poliomyelitis
  • Amyotrophic lateral sclerosis

Acute spinal cord injury (“spinal shock”)

  • Spinal cord compression or infarction
  • Disk herniation
  • Transverse myelitis
  • Occult spina bifida [6]


Symptoms of hyporeflexia include the inability to respond to stimuli applied to the knees, elbows or other areas. In some cases the reflex action may be totally absent. Hyporeflexia is itself typically a symptom of a larger problem that may be located in the spine. If you are experiencing slowed or non-existent reflexes, be sure to see your doctor for testing. Once the presence of hyporeflexia is established with reflex tests, additional testing and imaging will probably be necessary to pinpoint the root of the problem.[7]


Treatment options for hyporeflexia depend on exactly what is causing it. If the condition is caused by pressure to the spinal cord, physical therapy may be prescribed to alleviate this pressure. If that doesn't work, surgery can help clear any areas of nerve pressure, restoring order and stability to the spinal canal. To find out which course of treatment is best for your case of hyporeflexia, speak to a doctor who is familiar with the condition. At The Bonati Institute for Advanced Arthroscopic Surgery, a variety of treatments exist that may eliminated symptoms of hyporeflexia. The Bonati Institute was founded in 1981 and is renowned all over the world for its effective, highly successful, minimally invasive surgeries.[8]


Compression mononeuropathy (e.g. carpal tunnel syndrome) results in a pattern of neurological deficits distal to the site of nerve injury. Common causes include carpal tunnel syndrome, common peroneal nerve palsy and radial nerve palsy. Length-dependent peripheral neuropathy is associated with the classic ‘glove-and-stocking’ distribution of sensory, motor and reflex findings. Sensory, motor and reflex abnormalities progressively increase as more proximal nerve fibres are affected. Common causes include diabetes mellitus, alcohol and drugs.[9]

Radiculopathy In disorders of the nerve root, hyporeflexia or areflexia often coexist with positive or negative sensory findings in a dermatomal distribution. Diminished reflexes are largely due to dysfunction of the afferent limb of the reflex arc. In patients less than 45 years of age, the most common cause is intervertebral disc disease. In older patients the most common cause is spondylosis and osteophyte formation (see Table 5.20).

Table5.20 Reflex, motor and sensory findings in disorders…

Guillain–Barré syndrome Acute inflammatory demyelinating polyradiculopathy (Guillain–Barré syndrome) causes areflexia in the distribution of the affected nerve roots. An ascending pattern of lower motor neuron findings is characteristic (e.g. hypotonia, weakness, areflexia).

Disorders of the anterior horn cells Disorders of the anterior horn cells cause diminished reflexes due to dysfunction of the efferent limb of the reflex. Lower motor neuron findings are characteristic (e.g. wasting, fasciculations, hypotonia, weakness). Causes include motor neuron disease (e.g. amyotrophic lateral sclerosis), poliomyelitis and spinal muscular atrophy.

Hyperacute upper motor neuron injury Acute spinal cord injury in the cervical and upper thoracic cord may result in areflexia, flaccid paralysis, complete sensory loss and sympathetic autonomic dysfunction below the level of the injury, resulting in a clinical syndrome known as spinal shock. In the first 24 hours following spinal cord injury, spinal cord neurons are less excitable, likely due to decreased muscle spindle excitability and segmental input from afferent pathways caused by loss of tonic facilitation by gamma motor neurons.

Normal Variant Diffusely decreased or absent reflexes, in isolation, do not necessarily represent neurological disease. Decreased or absent reflexes are significant when accompanied by lower motor neuron signs (e.g. wasting, fasciculations, hypotonia, weakness), in instances of asymmetrical reflexes or with other focal neurological signs.[10]

Current Studies[edit]

In several studies of patients without known pre-existing neurological disease, 6–50% of patients lack bilateral ankle jerk reflexes despite reinforcement manoeuvres, and a small proportion of the population have generalised hyperreflexia. The clinical utility of reflex examination findings in detecting cervical and lumbosacral radiculopathy.[11]

See also[edit]


  1. ^ "Areflexia". TheFreeDictionary.com. 
  2. ^ "Spinal Cord Injury and Compression". Patient UK. 
  3. ^ McMahon, Mary (December 4, 2014). "What is Hyporeflexia?". In Shereen Skola. WiseGeek. Conjecture. 
  4. ^ Kahan, Scott; Redonda Miller; Ellen G. Smith (March 1, 2008). Signs and Symptoms (2nd ed.). Lippincott Williams & Wilkins. 
  5. ^ Dennis, Mark; William Talbot Bowen, Lucy Cho, (January 27, 2012). Mechanisms of Clinical Signs (1st ed.). Elsevier Australia. 
  6. ^ Kahan, Scott; Redonda Miller; Ellen G. Smith (March 1, 2008). Signs and Symptoms (2nd ed.). Lippincott Williams & Wilkins. 
  7. ^ "Hyporeflexia". 
  8. ^ "Hyporeflexia". 
  9. ^ Dennis, Mark; William Talbot Bowen, Lucy Cho, (January 27, 2012). Mechanisms of Clinical Signs (1st ed.). Elsevier Australia. 
  10. ^ Dennis, Mark; William Talbot Bowen, Lucy Cho, (January 27, 2012). Mechanisms of Clinical Signs (1st ed.). Elsevier Australia. 
  11. ^ Dennis, Mark; William Talbot Bowen, Lucy Cho, (January 27, 2012). Mechanisms of Clinical Signs (1st ed.). Elsevier Australia.