Neuro Lower Limb Flashcards
How might a UMN lesion affect tone in the lower limb
What about tone in case of LMN lesion
Increased (spasticity or rigidity) +/- ankle clonus
Decreased (hypotonia) or normal
How do UMN and LMN lesions affect plantar reflexes in the lower limb
UMN: Upgoing/extensor (Babinski positive)
LMN: Normal (downgoing/flexor) or mute (i.e. no movement)
What are the key sections of the lower limb neuro exam
Gather the appropriate equipment (Tendon hammer; Neurotip; Cotton wool; Tuning fork (128Hz))
Intro (WIPERQQ)
General Inspection
Gait
Romberg’s test
Tone/ ankle clonus
Power (Hip, knee, ankle, toes)
Reflexes (knee-jerk, ankle-jerk, plantar)
Sensation (dermatomes, light-touch, pin-prick, vibration, proprioception)
Coordination (heel-to-shin test)
Further assessments and investigations
What are the clinical signs you should look out for at the beginning of the lower limb neuro exam
Scars: may provide clues regarding previous spinal or lower limb surgery.
Wasting of muscles: suggestive of lower motor neuron lesions or disuse atrophy.
Tremor: there are several subtypes including resting tremor and intention tremor.
Fasciculations: small, local, involuntary muscle contraction and relaxation which may be visible under the skin. Associated with lower motor neuron pathology (e.g. amyotrophic lateral sclerosis).
Pseudoathetosis: abnormal writhing movements (typically affecting the fingers) caused by a failure of proprioception.
Chorea: brief, semi-directed, irregular movements that are not repetitive or rhythmic but appear to flow from one muscle to the next. Patients with Huntington’s disease typically present with chorea.
Myoclonus: brief, involuntary, irregular twitching of a muscle or group of muscles. All individuals experience benign myoclonus on occasion (e.g. whilst falling asleep) however persistent widespread myoclonus is associated with several specific forms of epilepsy (e.g. juvenile myoclonic epilepsy).
Tardive dyskinesia: involuntary, repetitive body movements which can include protrusion of the tongue, lip-smacking and grimacing. This condition can develop secondary to treatment with neuroleptic medications including antipsychotics and antiemetics.
Hypomimia: a reduced degree of facial expression associated with Parkinson’s disease.
Ptosis and frontal balding: typically associated with myotonic dystrophy.
Ophthalmoplegia
What objects should you look for around the bed before a lower limb neuro exam
Walking aids: the ability to walk can be impacted by a wide range of neurological pathology.
Prescriptions: prescribing charts or personal prescriptions can provide useful information about the patient’s recent medications.
What is important to remember when assessing gait
Patients with neurological disease are often at an increased risk of falls so make sure to remain close to the patient during the assessment so that you are able to intervene if required.
How do you assess gait
Ask the patient to walk to the end of the examination room and then turn and walk back whilst you observe their gait paying attention to:
Stance: a broad-based ataxic gait is typically associated with midline cerebellar pathology (e.g. a lesion in multiple sclerosis or degeneration of the cerebellar vermis secondary to chronic alcohol excess).
Stability: a staggering, slow and unsteady gait is typical of cerebellar pathology. In unilateral cerebellar disease, patients will veer towards the side of the lesion.
Arm swing: often absent or reduced in Parkinson’s disease (typically unilateral initially).
Steps: small, shuffling steps are characteristic of Parkinson’s disease. High-stepping may indicate the presence of foot drop.
Turning: patients with cerebellar disease will find the turning manoeuvre particularly difficult
How do you assess tandem gait
Why do we assess this
Ask the patient to walk to the end of the examination room and back with their heels to their toes (known as ‘tandem gait’). Heel-to-toe walking exacerbates underlying unsteadiness making it easier to identify more subtle ataxia.
Tandem gait is particularly sensitive at identifying dysfunction of the cerebellar vermis (e.g. alcohol-induced cerebellar degeneration). Difficulties with heel-to-toe walking may also suggest weakness of the flexors muscles of the leg or sensory ataxia.
What are the key gaits to look out for
ataxic
Parkinsonian
High-stepping
waddling
hemiparetic
spastic paraparesis
What is an ataxic gait
Ataxic gait: broad-based, unsteady and associated with either cerebellar pathology or sensory ataxia (e.g. vestibular or proprioceptive dysfunction). In the context of proprioceptive sensory ataxia, patients typically watch their feet intently to compensate for the proprioceptive loss. If a cerebellar lesion is present the patient may veer to the side of the lesion.
What is a Parkinsonian gait
small, shuffling steps, stooped posture and reduced arm swing (initially unilateral). The patient will require several small steps to turn around. The gait appears rushed (festinating) and may get stuck (freeze). Hand tremor may also be noticeable.
What is a high-stepping gait
can be unilateral or bilateral and is typically caused by foot drop (weakness of ankle dorsiflexion). The patient also won’t be able to walk on their heel(s).
What is a waddling gait
shoulders sway from side to side, legs lifted off ground with the aid of tilting the trunk. Waddling gait is commonly caused by proximal lower limb weakness (e.g. myopathy).
What is a hemiparetic gait
one leg held stiffly and swings round in an arc with each stride (circumduction). This type of gait is commonly associated with individuals who have had a stroke.
What is spastic paraparesis
similar to hemiparetic gait but bilateral, with both legs stiff and circumducting. The patient’s feet may be inverted and “scissor”.
This type of gait is typically associated with hereditary spastic paraplegia.
What does Romberg’s test assess
Romberg’s test is used to assess for loss of proprioceptive or vestibular function (known as sensory ataxia). The test does not assess cerebellar function and instead is used to quickly screen for evidence of sensory ataxia (i.e. non-cerebellar causes of balance issues).
What is Romberg’s test based on
Romberg’s test is based on the premise that a patient requires at least two of the following three senses to maintain balance whilst standing:
Proprioception: the awareness of one’s body position in space.
Vestibular function: the ability to know one’s head position in space.
Vision: the ability to see one’s position in space.
Romberg’s test involves removing the sense of vision by asking the patient to close their eyes. As a result, if the patient has a deficit in proprioception or vestibular function they will struggle to remain standing without visual input.
How do you perform Romberg’s test
- Position yourself within arms reach of the patient to allow you to intervene should they begin to fall.
- Ask the patient to put their feet together and keep their arms by their sides (be aware that patients with truncal ataxia may struggle to do this, however, this type of unsteadiness is not the same as a positive Romberg’s sign).
- Ask the patient to close their eyes.
How do you interpret Romberg’s test
Falling without correction is abnormal and referred to as a positive Romberg’s sign. This indicates unsteadiness is due to sensory ataxia (i.e. a deficit of proprioceptive or vestibular function, rather than cerebellar function). Causes of proprioceptive dysfunction include joint hypermobility (e.g. Ehlers-Danlos syndrome), B12 deficiency, Parkinson’s disease and ageing (known as presbypropria). Causes of vestibular dysfunction include vestibular neuronitis and Ménière’s disease.
Swaying with correction is not a positive result and often occurs in cerebellar disease due to truncal ataxia.
How do you assess lower limb tone
Leg roll and leg lift
Briefly assess tone in the muscle groups of the hip, knee and ankle on each leg, comparing each side as you go. Ask the patient to keep their legs fully relaxed throughout the assessment.
- With the patient lying on the examination couch, roll each leg to assess tone in the muscles responsible for the rotation of the hip.
- Lift each knee briskly off the bed (warning the patient first) and observe the movement of the leg. In patients with normal tone, the knee should rise whilst the heel remains in contact with the bed (the heel will typically lift off the bed if there is increased tone).
What is clonus
Clonus is a series of involuntary rhythmic muscular contractions and relaxations that is associated with upper motor neuron lesions of the descending motor pathways (e.g. stroke, multiple sclerosis, cerebral palsy).
How do you assess ankle clonus
- Position the patient’s leg so that the knee and ankle are slightly flexed, supporting the leg with your hand under their knee, so they can relax.
- Rapidly dorsiflex and partially evert the foot to stretch the gastrocnemius muscle.
- Keep the foot in this position and observe for clonus. Clonus is felt as rhythmic beats of dorsiflexion and plantarflexion. If more than 5 beats of clonus are present, this would be classed as an abnormal finding.
How do you assess power in hip flexion
Give the myotome and muscles assessed as well as instructions
Myotome assessed: L1/2
Muscles assessed: iliopsoas
Instructions: Ask the patient to raise their leg off the bed and apply downward resistance over the anterior thigh: “Lift your leg off the bed and don’t let me push your leg down.”
How do you assess power in hip extension
Give the myotome and muscles assessed as well as instructions
Myotome assessed: L5/S1/S2 (inferior gluteal nerve)
Muscles assessed: gluteus maximus
Instructions: Place your hand under the patient’s thigh and ask them to resist you trying to lift their leg: “Don’t let me lift your leg off the bed.”
