STUDY - Technical - New Dacian's Medicine
Muscle
Weakness, Abnormal Movements and Imbalance
(6)
Translation Draft
I'll continue yesterday's post about imbalance and abnormal gait...
The imbalance with vestibular dysfunction is characterized by a constant tendency to fall to one side. The patient frequently accuses vertigo rather than imbalance, especially if the onset is acute. Acute vertigo associated with lateralized imbalance but without other neurological signs is often due to semicircular canal disorders, while the presence of other neurological signs suggests cerebral stem ischemia or myelinising disease.
When vestibular dysfunction is peripheral, positional nystagmus and vertigo tend to resolve if a provocative position is maintained (disappearance) or repeated (usual). Lateralized imbalance with progressive onset or persisting for more than 2 weeks, accompanied by nystagmus, may result from damage to the semicircular canal or vestibular nerve, brain stem or cerebellum.
The imbalance with sensory ataxia is characterized by marked worsening when the visual feedback is removed. The patient can frequently approach the vertical position with his feet glued with caution, with his eyes open. When closing the eyes, the balance is quickly lost (positive Romberg sign) in different directions, at random.
Sensory examination reveals impairment of the proprioceptivity of the toes and ankles, usually associated with an even more pronounced abnormality of vibrating perception. Prompt assessment of vitamin B12 deficiency is important as this condition is reversible if recognised early on. Depression or the absence of reflexes reveal peripheral nerve disorders.
Spasticity with plantar extensor responses suggests damage to the posterior cord and spinal cord. Rarely, sensory ataxia produces lateralized imbalance. In these cases the condition is usually in the parietal lobe or thalamus, but may also be due to asymmetric sensory neuropathy or posterior cord disease.
Sensory ataxia of the limbs is similar to cerebellar ataxia of the limbs, but is accentuated when the eyes are closed. The examination also reveals proprioceptive perceptions and abnormal vibrators. The approach will focus on locating proprioceptive damage to peripheral nerves, posterior cords of the spinal cord or less often to the parietal lobe.
There are other forms of imbalance (and I will no longer present them in this post) but the fundamental problem is usually of primary impairment of force, pyramidal function or cortical initiation of movement. I'm going to switch to abnormal gait now.
Each of the dysfunctions discussed so far produces a characteristic impairment of gait. If neurological examination is normal, except abnormal gait, diagnosis can be difficult even for an experienced clinician.
Hemiparetic gait characterizes spastic hemiparesis. In its most severe form, an abnormal position of the limbs is produced by spasticity. The shoulder is in the abstraction and internal rotation, with the flexion of the elbow, wrist and fingers and with the extension of the hip, knee and ankle.
The forward swaying of the spastic leg during walking requires the abduction and circumduction of the hip, frequently with the contralateral bending of the torso. In the lightest form, the affected arm is held in a normal position but swings less than the normal arm. The affected leg is less flexed than the normal leg during the forward swing and is more externally rotated. A hemiparetic gait is a common residual result of a stroke.
Paraparetic walking is a type of gait in which both legs are moved in a slow, rigid, circumductional manner, similar to the movement of the legs in the hemiparetic gait. In many patients the legs tend to cross with each swing in the face (shearing movement). A parparatic gait is a common sign of spinal cord disease and also occurs in cerebral palsy.
Stepped walking is caused by damage to the ankle dorsoflexia. Due to partial or complete fall of the foot, the lower limb should be raised higher than usual to avoid catching the floor halucle during the front swing of the lower limb. If it is unilateral, steppe dining is usually due to L5 radiculopathy, sciatic neuropathy or peroneal neuropathy. If bilateral, it is the usual result of distal polyneuropathy or lombosacrate radiculopathy.
The swaying gait results from the proximal weakness of the lower limb, very commonly due to myopathy and occasionally the disease of the neuromuscular junction or proximal symmetrical spinal muscular atrophy.
Due to damage to the hip flexion, the torso is tilted away from the foot that is moved to lift the hip and provides an additional distance between the leg and the floor, and the pelvis is rotated forward to help move forward the leg. Since the weakness of the pelvic belt is usually bilateral, the lifting and rotation of the pelvis alternates from side to side, giving the gait the swaying appearance.
Parkinson's gait is characterized by a forward bending, with modest flexion of the hips and knees. The arms are flexed at the elbows and brought to the shoulders, often with a 4 to 6 Hz resting pronation-sigh tremor, but affect sfewofi other movements even while walking. Walking is slowly initiated by bending forward and maintained with fast short steps, while the legs are dragged along the floor.
The step tends to accelerate as the upper body tilts more before the legs, whether the movement is forward (propulsion) or backward (retropulsion). Postural instability leads to falls.
Apraxic gait results from bilateral frontal lobe disease, with impaired ability to plan and execute sequential movements. This gait is superficially similar to that of parkinsonism, in that the posture is tilted and all the steps are short and dragged.
However, the initiation and maintenance of walking are affected in a different way. Every movement that is necessary for walking can usually be performed if it is tested in isolation while the patient is sitting down or lying down. However, when the patient is asked to step forward when standing, a long pause often occurs before any attempt to flex the hip and move forward.
Moreover, once walking is initiated, it is not maintained, even proceeding in an abnormal, accelerated manner. Rather, after one or more steps are taken, the walk is stopped for a few seconds or more. This process is then repeated. This gait is usually accompanied by dementia.
The choreoatetosistal gait is characterized by an intermittent, irregular movement, which interrupts the quiet flow of a normal gait. Flexion or hip extension movements are common and unforeseeable, but observed as a pelvic wobble.
Ataxic cerebellar walking is a condition of wide-based walking in which the speed and length of the step vary irregularly from step to step. In middle cerebellar disease, as in alcoholics, the posture is vertical, but the legs are separated and the ataxia of the lower limb is also commonly present. Taking a particular position or changing the position can cause instability, however the balance can usually be maintained with open or closed eyes.
Walking can be fast, but the cadence is irregular. Although patients usually do not have confidence in the stability of their gait, minimal support is often necessary for safety. In cerebellar hemisphere disease, limb ataxia and nystagmus are usually also present.
Sensory ataxic walking can resemble cerebellar walking, its wide-base position and difficulty changing position. However, although balance can be maintained with open eyes, loss of visual appearance by closing the eyes causes rapid loss of balance with a fall (positive Romberg sign) if the examiner does not help the patient.
The vestibular gait is where the patient constantly tends to fall to one side, whether it's walking or sitting. Examination of the cranial nerves demonstrates an obvious asymmetrical nystagmus. The possibilities of unilateral sensory ataxia and hemiparesis are excluded by the signs of proprioceptivity and normal power.
Today-abazia is a typical histrionic condition of walking. Although the patient usually has normal coordination of lower limb movements in bed or while sitting down, he is unable to stand or walk without help. if distracted, the stationary balance is sometimes maintained and a few steps are taken normally, before a dramatic demonstration of imbalance with the headof to the examiner's arms or to any nearby support point.
And I'm done with this section of the disease signs. In the following posts I will address spasms, muscle cramps and episodic muscle weakness under the title "Spasms and cramps".
I apologize for the laconic expression but I'm having a hard day and I couldn't afford to have time for some details. I hope it doesn't happen again, but... life must be lived as it is... Sorry again!
I'll continue yesterday's post about imbalance and abnormal gait...
The imbalance with vestibular dysfunction is characterized by a constant tendency to fall to one side. The patient frequently accuses vertigo rather than imbalance, especially if the onset is acute. Acute vertigo associated with lateralized imbalance but without other neurological signs is often due to semicircular canal disorders, while the presence of other neurological signs suggests cerebral stem ischemia or myelinising disease.
When vestibular dysfunction is peripheral, positional nystagmus and vertigo tend to resolve if a provocative position is maintained (disappearance) or repeated (usual). Lateralized imbalance with progressive onset or persisting for more than 2 weeks, accompanied by nystagmus, may result from damage to the semicircular canal or vestibular nerve, brain stem or cerebellum.
The imbalance with sensory ataxia is characterized by marked worsening when the visual feedback is removed. The patient can frequently approach the vertical position with his feet glued with caution, with his eyes open. When closing the eyes, the balance is quickly lost (positive Romberg sign) in different directions, at random.
Sensory examination reveals impairment of the proprioceptivity of the toes and ankles, usually associated with an even more pronounced abnormality of vibrating perception. Prompt assessment of vitamin B12 deficiency is important as this condition is reversible if recognised early on. Depression or the absence of reflexes reveal peripheral nerve disorders.
Spasticity with plantar extensor responses suggests damage to the posterior cord and spinal cord. Rarely, sensory ataxia produces lateralized imbalance. In these cases the condition is usually in the parietal lobe or thalamus, but may also be due to asymmetric sensory neuropathy or posterior cord disease.
Sensory ataxia of the limbs is similar to cerebellar ataxia of the limbs, but is accentuated when the eyes are closed. The examination also reveals proprioceptive perceptions and abnormal vibrators. The approach will focus on locating proprioceptive damage to peripheral nerves, posterior cords of the spinal cord or less often to the parietal lobe.
There are other forms of imbalance (and I will no longer present them in this post) but the fundamental problem is usually of primary impairment of force, pyramidal function or cortical initiation of movement. I'm going to switch to abnormal gait now.
Each of the dysfunctions discussed so far produces a characteristic impairment of gait. If neurological examination is normal, except abnormal gait, diagnosis can be difficult even for an experienced clinician.
Hemiparetic gait characterizes spastic hemiparesis. In its most severe form, an abnormal position of the limbs is produced by spasticity. The shoulder is in the abstraction and internal rotation, with the flexion of the elbow, wrist and fingers and with the extension of the hip, knee and ankle.
The forward swaying of the spastic leg during walking requires the abduction and circumduction of the hip, frequently with the contralateral bending of the torso. In the lightest form, the affected arm is held in a normal position but swings less than the normal arm. The affected leg is less flexed than the normal leg during the forward swing and is more externally rotated. A hemiparetic gait is a common residual result of a stroke.
Paraparetic walking is a type of gait in which both legs are moved in a slow, rigid, circumductional manner, similar to the movement of the legs in the hemiparetic gait. In many patients the legs tend to cross with each swing in the face (shearing movement). A parparatic gait is a common sign of spinal cord disease and also occurs in cerebral palsy.
Stepped walking is caused by damage to the ankle dorsoflexia. Due to partial or complete fall of the foot, the lower limb should be raised higher than usual to avoid catching the floor halucle during the front swing of the lower limb. If it is unilateral, steppe dining is usually due to L5 radiculopathy, sciatic neuropathy or peroneal neuropathy. If bilateral, it is the usual result of distal polyneuropathy or lombosacrate radiculopathy.
The swaying gait results from the proximal weakness of the lower limb, very commonly due to myopathy and occasionally the disease of the neuromuscular junction or proximal symmetrical spinal muscular atrophy.
Due to damage to the hip flexion, the torso is tilted away from the foot that is moved to lift the hip and provides an additional distance between the leg and the floor, and the pelvis is rotated forward to help move forward the leg. Since the weakness of the pelvic belt is usually bilateral, the lifting and rotation of the pelvis alternates from side to side, giving the gait the swaying appearance.
Parkinson's gait is characterized by a forward bending, with modest flexion of the hips and knees. The arms are flexed at the elbows and brought to the shoulders, often with a 4 to 6 Hz resting pronation-sigh tremor, but affect sfewofi other movements even while walking. Walking is slowly initiated by bending forward and maintained with fast short steps, while the legs are dragged along the floor.
The step tends to accelerate as the upper body tilts more before the legs, whether the movement is forward (propulsion) or backward (retropulsion). Postural instability leads to falls.
Apraxic gait results from bilateral frontal lobe disease, with impaired ability to plan and execute sequential movements. This gait is superficially similar to that of parkinsonism, in that the posture is tilted and all the steps are short and dragged.
However, the initiation and maintenance of walking are affected in a different way. Every movement that is necessary for walking can usually be performed if it is tested in isolation while the patient is sitting down or lying down. However, when the patient is asked to step forward when standing, a long pause often occurs before any attempt to flex the hip and move forward.
Moreover, once walking is initiated, it is not maintained, even proceeding in an abnormal, accelerated manner. Rather, after one or more steps are taken, the walk is stopped for a few seconds or more. This process is then repeated. This gait is usually accompanied by dementia.
The choreoatetosistal gait is characterized by an intermittent, irregular movement, which interrupts the quiet flow of a normal gait. Flexion or hip extension movements are common and unforeseeable, but observed as a pelvic wobble.
Ataxic cerebellar walking is a condition of wide-based walking in which the speed and length of the step vary irregularly from step to step. In middle cerebellar disease, as in alcoholics, the posture is vertical, but the legs are separated and the ataxia of the lower limb is also commonly present. Taking a particular position or changing the position can cause instability, however the balance can usually be maintained with open or closed eyes.
Walking can be fast, but the cadence is irregular. Although patients usually do not have confidence in the stability of their gait, minimal support is often necessary for safety. In cerebellar hemisphere disease, limb ataxia and nystagmus are usually also present.
Sensory ataxic walking can resemble cerebellar walking, its wide-base position and difficulty changing position. However, although balance can be maintained with open eyes, loss of visual appearance by closing the eyes causes rapid loss of balance with a fall (positive Romberg sign) if the examiner does not help the patient.
The vestibular gait is where the patient constantly tends to fall to one side, whether it's walking or sitting. Examination of the cranial nerves demonstrates an obvious asymmetrical nystagmus. The possibilities of unilateral sensory ataxia and hemiparesis are excluded by the signs of proprioceptivity and normal power.
Today-abazia is a typical histrionic condition of walking. Although the patient usually has normal coordination of lower limb movements in bed or while sitting down, he is unable to stand or walk without help. if distracted, the stationary balance is sometimes maintained and a few steps are taken normally, before a dramatic demonstration of imbalance with the headof to the examiner's arms or to any nearby support point.
And I'm done with this section of the disease signs. In the following posts I will address spasms, muscle cramps and episodic muscle weakness under the title "Spasms and cramps".
I apologize for the laconic expression but I'm having a hard day and I couldn't afford to have time for some details. I hope it doesn't happen again, but... life must be lived as it is... Sorry again!
Have
a good, fruitful week, full of understanding, love and
gratitude!
Dorin, Merticaru