UMN/LMN SYNDROMES

Dr Gavin Ng Emergency Physician

Peer review: Dr David McCreary

THE CASE A 23-year-old gentleman presents to your Emergency Department with the complaint of difficulty walking. He has other medical history, and takes no regular medications. He is somewhat overweight, but maintains a balanced diet.

The following history is provided:

1. Difficulty walking over the last 4 months

   1. Describes mainly losing balance and falling over once.

   2. Associated with gradual onset back pain, which the patient attributes to lifting at work.

   3. Has attended a physiotherapy session, who has recommended he present to ED for a medical opinion.

2. Describes pins and needles in the right leg, in comparison to the left.

3. Confirms the following:

   1. No episodes of bladder or bowel incontinence

   2. No loss of saddle sensation

   3. No history of trauma to the back.

The lower limb neurological exam is detailed below:

Lower limb neurological exam

	Right	Left
Tone	Normal Clonus present in ankle (10 beats)	Normal Clonus present in ankle (8 beats)
Power	4+/5 in hip flexion Otherwise. 5/5 power in other hip, knee and ankle movements.	4+/5 in hip flexion Otherwise, 5/5 power in other hip, knee and ankle movements.
Reflexes	Knee jerk - hyperreflexia present	Knee jerk - hyperreflexia present
Sensation	Normal sensation is present	Normal sensation is present

Otherwise, the upper limb examination, cerebellar examination and cranial nerve examination is unremarkable. He has intact saddle sensation and intact anal tone.

QUESTION 1: HOW DO WE CLASSIFY NEUROLOGICAL COMPLAINTS IN THE ED?

Motor neurological complaints may be classified as either upper motor neuron (UMN) syndromes or lower motor neuron (LMN) syndromes, based on their clinical findings.

1. Lesions to UMN or LMN areas produce distinct clinical features that may help identify the location and thus assist with decision making, e.g. imaging choices.

QUESTION 2: WHAT ARE UMNS AND LMNS?

1. UMNs are neurons that are responsible for initiation and inhibition of movement. They originate in the cortex, travel to the ipsilateral medulla where they decussate to form the contralateral corticospinal tract.

   1. They terminate at the anterior horn, where they synapse with a LMN.

2. LMNs are neurons that connect the UMN to the effector cell.

Figure 1: demonstrating the location of both UMNs and LMNs (Case courtesy of OpenStax College, Radiopaedia.org, rID: 53266)

QUESTION 3: WHAT EXAMINATION FINDINGS ARE ASSOCIATED WITH UMN AND LMN SYNDROMES?

1. As the UMNs are associated with initiation and inhibition of movement, this syndrome produces both positive and negative features.

2. LMN syndromes predominantly have negative features.

3. The table below provides a summary of the expected examination findings:

	UMN Syndrome	LMN Syndrome
Tone	Hypertonia Spasticity	Hypotnia
Power	Weakness present	Weakness present Flaccid paralysis
Reflexes	Hyperreflexia Clonus Upgoing Babinski Reflex	Hyporeflexia
Others	Impaired motor control Easy fatigability Loss of dexterity	Muscle wasting Fasciculations

QUESTION 4: WHAT ARE THE POTENTIAL CAUSES OF UMN AND LMN SYNDROMES?

1. As the UMN travels from the cortex through the cortico-spinal tract, any injury before the anterior horn will produce an UMN syndrome.

   1. Remember that as discussed above, as the decussation occurs at the level of the medulla, lesions above the medulla will present with contra-lateral signs and lesions below the medulla will present with ipsilateral signs.

   2. Some examples of lesions that can produce an UMN syndrome are:

      1. Brain lesions – strokes; traumatic brain injury; anoxic brain injury

      2. Spinal cord lesions – MS; transverse myelitis; amyotrophic lateral sclerosis

2. LMN syndromes occur when there is injury to the anterior horn cells, or the peripheral nerve.

   1. A disorder at the neuromuscular junction (E.g., myasthenia gravis) may mimic a LMN syndrome as well.

QUESTION 5: WHAT DO THE HISTORY AND EXAMINATION FEATURES SUGGEST?

An upper motor neuron (UMN) syndrome; suggestive of a spinal cord lesion.

• The lesion is probably in the thoraco-lumbar region, given the absence of clinical findings in the head, neck and upper limbs.

QUESTION 6: COULDN'T THIS BE CAUDA EQUINA SYNDROME (CES)?

1. CES is worth mentioning here, as it should be on the list of differentials for all patients presenting to the ED with back pain and lower limb neurological complaints.

2. However, remember that CES presents as a LMN syndrome, with bladder and bowel dysfunction. This is in contrast to our patient’s presentation.

3. The key features of CES are(1):

   1. Lower back pain, with pain radiating down one or both legs.

   2. Weakness – weakness in plantar flexion suggests S1-S2 nerve root involvement

   3. Hyporeflexia – loss of ankle jerks suggests S1-S2 nerve root involvement.

   4. Bladder and rectal sphincter paralysis

      1. The most common symptom is urinary retention(2).

   5. Loss of sensation in the saddle area.

OUTCOME

Given the clinical findings, the patient was admitted to the neurology ward for further investigation.

• MRI Brain and MRI Spine was performed, which demonstrated multi-level spinal canal stenosis in the thoracic spine, secondary to osteophyte formation. There was also evidence of cord myelopathy at T1-T2 region.

• He was then referred on to the spinal surgery team for definitive fixation.

REFERENCES

1. Eisen A. Anatomy and localization of spinal cord disorders In: Aminoff M, editor. UpToDate. UpToDate, Waltham, MA

2. Wiseman D. Cauda Equina Syndrome https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Cauda-Equina-Syndrome.=">https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Cauda-Equina-Syndrome</a>.">Gavin Ng is a Fellow of the Australasian College for Emergency Medicine, and is currently employed as an Emergency Physician at Alfred Health and Ballarat Health Services.
   

GAVIN NG

Emergency Physician

Gavin Ng is a Fellow of the Australasian College for Emergency Medicine, and is currently employed as an Emergency Physician at Alfred Health and Ballarat Health Services. Gavin has completed his undergraduate medical training in 2011, graduating from the University of Melbourne. He has been training in Emergency Medicine since 2014. Gavin has worked in a variety of clinical settings, ranging from metropolitan EDs to regional areas in Victoria. His clinical interests are Critical Care Medicine and Trauma medicine, and he has previous experience working as a Trauma Fellow at Alfred Health. He is also a current ALS2 (Advanced Life Support Level 2) instructor. He also has a passion for education – he has previously been involved in teaching junior medical staff through the Northern Clinical School.