STUDY - Technical - New Dacian's Medicine
Muscle
Weakness, Abnormal Movements and Imbalance
(3)
Translation Draft
Let's move on with this "area" of manifestation of the signs of the disease.
Paraparesis most commonly results from an intraspinal lesion in or below the upper thoracic spine. A sensory level on the trunk identifies the approximate level of spinal injury. Other causes of paraparesis include other central motor neuron lesions (parasagital lesions and hydrocephalus) and peripheral motor neuron lesions (previous horn cell disorders, horsetail syndrome and atypical peripheral neuropathies).
Acute paraparesis due to a disease of the spinal cord can be difficult to distinguish from conditions targeting peripheral motor neurons or cerebral hemispheres. In paraparesis or paraplegia from acute spinal cord disease, central motor neuron deficiency is usually associated with urinary and fecal incontinence and often with numbness of the lower limb, which extends cranially to a certain level of the torso (the tone is typical flasc and tendon reflexes are absent).
With a sensory level and sphincter involvement, the diagnostic approach begins with an imaging study of the spinal cord. Diagnostic possibilities include epidural metastases, epidural hematoma and spinal cord ischemia due to a dural arteriovenous fistula or other vascular abnormality, each of which requires immediate intervention. They must be differentiated from transverse myelitis and lesions outside the spine.
Diseases of the cerebral hemispheres that cause acute paraparesis include ischemia of the anterior cerebral artery, thrombosis of the upper sagittal sinus, cortical venous thrombosis or acute hydrocephalus. If the signs of the central motor neuron are associated with drowsiness, confusion, seizures or other cortical signs, but not with a sensory level above the torso, the diagnostic approach begins with a cerebral MRI.
Paraparesis is part of horsetail syndrome that can result from lower spine trauma, middle-line disc hernia or lumbar intraspinal metastases (although sphincters are affected, hip flexion is commonly felt as a sensation on the anterolateral face of the thighs). Paraparesis is rarely caused by acute demyelinating polyneuropathy (the most common form of Guillain-Barre syndrome) or rarely by myopathy. In such cases, electrophysiological studies help diagnosis and reorient subsequent evaluation.
Subacute or chronic paraparesis with spasticity is caused by central motor neuron disease. When paraparesis develops in weeks or months, with loss of lower limb sensitivity and sphincteral interest, possible diseases of the marrow include multiple sclerosis, intraparenchymal tumors, chronic compression of the spinal cord due to degenerative disease of the marrow, combined subacute degeneration due to vitamin B12 deficiency and hereditary diseases.
Chronic progressive multiple sclerosis usually occurs in the fourth or fifth decade, with progressive paraparesis. Primary gliomas of the spinal cord typically produce a progressive myelopathy, which is painful. The clinical approach begins with MRI or a myelography for viewing the spinal cord. If the imaging study is normal and spasticity is present, brain MRI may also be indicated.
If cortical signs are present, parasagital meningioma or chronic hydrocephalus are probable and brain MRI is the initial test. Progression from months to years may also be due to degenerative conditions such as primary lateral sclerosis or hereditary conditions such as familial spastic paraparesis and adenomyeloneuropatia.
In rare situations where chronic paraparesis is due to peripheral motor neuron dysfunction or myopathic weakness, localization is usually suspected on the basis of clinical signs and is confirmed by EMG and nerve driving tests.
Quadriparesis may result from central motor neuron disease (located in the upper cervical spinal cord or above), diffuse peripheral motor neuron disease or myopathy.
Acute quadriparesis with onset within minutes includes in differential diagnosis many diseases of central motor neurons (e.g. anoxia, hypotension, ischemia of the brain stem or cervical marrow, trauma and systemic metabolic abnormalities) and also rare forms of myopathic weakness (systemic toxins or periodic paralysis).
The onset in hours to several days may be due to disorders of the central motor neuron, peripheral motor neuron or myopathic neuron. All three types of weakness are initially associated, usually with hypotonia. If acute quadriparesis is associated with stupor or coma, evaluation begins with a cerebral TC.
If the signs of the central neuron are present, but the patient is vigil, the initial test is usually an MRI of the spine. If the weakness is of a peripheral motor neuron, myopathic or of unknown origin, the clinical approach begins with an electrodiagnostic study. Acute demyelinating polyneuropathy is an important diagnostic possibility in this situation.
When quadriparesis due to central motor neuron disease occurs within a few weeks, months or years, the distinction between disorders of the cerebral hemispheres, brain stem and cervical spinal cord is usually possible only by clinical criteria. The diagnostic approach begins with an MRI of the clinical site suspected to be pathological. Peripheral motor neuron disease presents with a weakness that is the deepest distal, while myopathic weakness is typically proximal. The evaluation then begins with an EMG and nervous driving studies.
Monoparesis or weakness of a single limb is usually due to peripheral motor neuron disease, with or without associated sensory involvement. Central motor neuron dysfunction is occasionally presented with distal and nonantigravity muscle monoparesis. Myopathic damage is rarely limited to a single limb. Acute monoparesis is difficult to "delimited" because the distinction between central and peripheral neuron disorders can be difficult only by motor examination, since tone and reflexes are frequently low in both situations during acute episode.
If weakness is predominant in distal and nonantigravity muscles and is not associated with sensory impairment or pain, focal cortical ischemia is likely (in this situation the diagnostic possibilities are similar to those for acute hemiparesis). Acute peripheral motor neuron disease is usually accompanied by sensory loss and pain.
The distribution of weakness is commonly located at a single nerve root or peripheral nerve within a limb. If weakness of peripheral motor nerve is suspected or if the type of weakness is uncertain, the clinical approach begins with EMG and a nerve driving study. Subacute or chronic monoparesis or segmental impairment has various manifestations.
The weakness or atrophy of a single limb, which develops in weeks or months, is almost always due to a localized impairment of peripheral motor neurons. If weakness is associated with numbness, the origin is likely in the peripheral nerve or spinal root (unusually the brachial and lombosacrat plexuses are affected). if numbness is absent, segmental disease of anterior horn cells is likely.
In each of the cases an electrodiagnostic study is indicated. If the signs of the central motor neuron are present rather than the signs of peripheral motor neuron, the cause may be a tumor, vascular malformation or other cortical lesion affecting the precentral gyrus. Alternatively, if the lower limb is affected, a small lesion of the thoracic marrow, frequently a tumor or demyelinating plaque, may be present. In these situations, the approach begins with an imaging study of the suspected area.
It's the turn of distal weakness. The distal interest of two or four limbs suggests peripheral motor neuron disease or peripheral nerve. Acute distal weakness of the lower limb occasionally occurs from acute toxic polyneuropathy or from u ponytail syndrome. Distal symmetrical weakness usually occurs in weeks, months or years and is due to metabolic, toxic, hereditary, degenerative or inflammatory diseases of peripheral nerves.
In peripheral nerve disease, weakness is usually less severe than numbness. Anterior horn cell disease may start distal, but it is typically asymmetrical and not associated with numbness. Rarely, myopathy also presents with distal weakness, without associated numbness. The first step in evaluation is to obtain an electrodiagnostic study.
The proximal weakness of two or four limbs suggests dysfunction of the muscle or, less commonly, of the neuromuscular junction or anterior horn cells. Proximal weakness that develops in weeks, months or years is usually due to hereditary, inflammatory, metabolic or endocrine diseases.
Myopathy frequently produces symmetrical weakness of the pelvic or scapular belt muscles. Neuromuscular junction diseases (such as myasthenia gravis) can be manifested by symmetrical proximal weakness, commonly associated with ptosis, diplopia or bulbar weakness and fluctuating as severity during the day. Proximal weakness in anterior horn cell disease is very frequently asymmetrical, but can be symmetrical if it is familial.
Numbness does not occur in any of these diseases. Evaluation usually begins with the determination of serum creatikinase levels and electrophysiological studies.
I will complete this post by actually making an introduction to the next one, where I will discuss the dysfunctions of the movement.
Movement dysfunctions are neurological syndromes in which abnormal movements (or dyskinesis) occur due to a disturbance of fluency and speed of voluntary movement or due to the presence of additional unintentional movement. Because they are so distinct from the pyramidal disorders that cause weakness due to the central motor neuron, motion dysfunctions are commonly referred to as extrapyramidal diseases.
Motion dysfunctions are divided into two types, hypokinetic and hyperkinetic. Hypokinetic movement dysfunctions are characterized by akinesis or bradykinesis, in which the proposed motor activity is absent or reduced. This is commonly described as a "poor movement". Hyperkinetic dysfunctions of movement are those in which an excessive amount of spontaneous motor activity is observed or abnormal involuntary movements occur.
Let's move on with this "area" of manifestation of the signs of the disease.
Paraparesis most commonly results from an intraspinal lesion in or below the upper thoracic spine. A sensory level on the trunk identifies the approximate level of spinal injury. Other causes of paraparesis include other central motor neuron lesions (parasagital lesions and hydrocephalus) and peripheral motor neuron lesions (previous horn cell disorders, horsetail syndrome and atypical peripheral neuropathies).
Acute paraparesis due to a disease of the spinal cord can be difficult to distinguish from conditions targeting peripheral motor neurons or cerebral hemispheres. In paraparesis or paraplegia from acute spinal cord disease, central motor neuron deficiency is usually associated with urinary and fecal incontinence and often with numbness of the lower limb, which extends cranially to a certain level of the torso (the tone is typical flasc and tendon reflexes are absent).
With a sensory level and sphincter involvement, the diagnostic approach begins with an imaging study of the spinal cord. Diagnostic possibilities include epidural metastases, epidural hematoma and spinal cord ischemia due to a dural arteriovenous fistula or other vascular abnormality, each of which requires immediate intervention. They must be differentiated from transverse myelitis and lesions outside the spine.
Diseases of the cerebral hemispheres that cause acute paraparesis include ischemia of the anterior cerebral artery, thrombosis of the upper sagittal sinus, cortical venous thrombosis or acute hydrocephalus. If the signs of the central motor neuron are associated with drowsiness, confusion, seizures or other cortical signs, but not with a sensory level above the torso, the diagnostic approach begins with a cerebral MRI.
Paraparesis is part of horsetail syndrome that can result from lower spine trauma, middle-line disc hernia or lumbar intraspinal metastases (although sphincters are affected, hip flexion is commonly felt as a sensation on the anterolateral face of the thighs). Paraparesis is rarely caused by acute demyelinating polyneuropathy (the most common form of Guillain-Barre syndrome) or rarely by myopathy. In such cases, electrophysiological studies help diagnosis and reorient subsequent evaluation.
Subacute or chronic paraparesis with spasticity is caused by central motor neuron disease. When paraparesis develops in weeks or months, with loss of lower limb sensitivity and sphincteral interest, possible diseases of the marrow include multiple sclerosis, intraparenchymal tumors, chronic compression of the spinal cord due to degenerative disease of the marrow, combined subacute degeneration due to vitamin B12 deficiency and hereditary diseases.
Chronic progressive multiple sclerosis usually occurs in the fourth or fifth decade, with progressive paraparesis. Primary gliomas of the spinal cord typically produce a progressive myelopathy, which is painful. The clinical approach begins with MRI or a myelography for viewing the spinal cord. If the imaging study is normal and spasticity is present, brain MRI may also be indicated.
If cortical signs are present, parasagital meningioma or chronic hydrocephalus are probable and brain MRI is the initial test. Progression from months to years may also be due to degenerative conditions such as primary lateral sclerosis or hereditary conditions such as familial spastic paraparesis and adenomyeloneuropatia.
In rare situations where chronic paraparesis is due to peripheral motor neuron dysfunction or myopathic weakness, localization is usually suspected on the basis of clinical signs and is confirmed by EMG and nerve driving tests.
Quadriparesis may result from central motor neuron disease (located in the upper cervical spinal cord or above), diffuse peripheral motor neuron disease or myopathy.
Acute quadriparesis with onset within minutes includes in differential diagnosis many diseases of central motor neurons (e.g. anoxia, hypotension, ischemia of the brain stem or cervical marrow, trauma and systemic metabolic abnormalities) and also rare forms of myopathic weakness (systemic toxins or periodic paralysis).
The onset in hours to several days may be due to disorders of the central motor neuron, peripheral motor neuron or myopathic neuron. All three types of weakness are initially associated, usually with hypotonia. If acute quadriparesis is associated with stupor or coma, evaluation begins with a cerebral TC.
If the signs of the central neuron are present, but the patient is vigil, the initial test is usually an MRI of the spine. If the weakness is of a peripheral motor neuron, myopathic or of unknown origin, the clinical approach begins with an electrodiagnostic study. Acute demyelinating polyneuropathy is an important diagnostic possibility in this situation.
When quadriparesis due to central motor neuron disease occurs within a few weeks, months or years, the distinction between disorders of the cerebral hemispheres, brain stem and cervical spinal cord is usually possible only by clinical criteria. The diagnostic approach begins with an MRI of the clinical site suspected to be pathological. Peripheral motor neuron disease presents with a weakness that is the deepest distal, while myopathic weakness is typically proximal. The evaluation then begins with an EMG and nervous driving studies.
Monoparesis or weakness of a single limb is usually due to peripheral motor neuron disease, with or without associated sensory involvement. Central motor neuron dysfunction is occasionally presented with distal and nonantigravity muscle monoparesis. Myopathic damage is rarely limited to a single limb. Acute monoparesis is difficult to "delimited" because the distinction between central and peripheral neuron disorders can be difficult only by motor examination, since tone and reflexes are frequently low in both situations during acute episode.
If weakness is predominant in distal and nonantigravity muscles and is not associated with sensory impairment or pain, focal cortical ischemia is likely (in this situation the diagnostic possibilities are similar to those for acute hemiparesis). Acute peripheral motor neuron disease is usually accompanied by sensory loss and pain.
The distribution of weakness is commonly located at a single nerve root or peripheral nerve within a limb. If weakness of peripheral motor nerve is suspected or if the type of weakness is uncertain, the clinical approach begins with EMG and a nerve driving study. Subacute or chronic monoparesis or segmental impairment has various manifestations.
The weakness or atrophy of a single limb, which develops in weeks or months, is almost always due to a localized impairment of peripheral motor neurons. If weakness is associated with numbness, the origin is likely in the peripheral nerve or spinal root (unusually the brachial and lombosacrat plexuses are affected). if numbness is absent, segmental disease of anterior horn cells is likely.
In each of the cases an electrodiagnostic study is indicated. If the signs of the central motor neuron are present rather than the signs of peripheral motor neuron, the cause may be a tumor, vascular malformation or other cortical lesion affecting the precentral gyrus. Alternatively, if the lower limb is affected, a small lesion of the thoracic marrow, frequently a tumor or demyelinating plaque, may be present. In these situations, the approach begins with an imaging study of the suspected area.
It's the turn of distal weakness. The distal interest of two or four limbs suggests peripheral motor neuron disease or peripheral nerve. Acute distal weakness of the lower limb occasionally occurs from acute toxic polyneuropathy or from u ponytail syndrome. Distal symmetrical weakness usually occurs in weeks, months or years and is due to metabolic, toxic, hereditary, degenerative or inflammatory diseases of peripheral nerves.
In peripheral nerve disease, weakness is usually less severe than numbness. Anterior horn cell disease may start distal, but it is typically asymmetrical and not associated with numbness. Rarely, myopathy also presents with distal weakness, without associated numbness. The first step in evaluation is to obtain an electrodiagnostic study.
The proximal weakness of two or four limbs suggests dysfunction of the muscle or, less commonly, of the neuromuscular junction or anterior horn cells. Proximal weakness that develops in weeks, months or years is usually due to hereditary, inflammatory, metabolic or endocrine diseases.
Myopathy frequently produces symmetrical weakness of the pelvic or scapular belt muscles. Neuromuscular junction diseases (such as myasthenia gravis) can be manifested by symmetrical proximal weakness, commonly associated with ptosis, diplopia or bulbar weakness and fluctuating as severity during the day. Proximal weakness in anterior horn cell disease is very frequently asymmetrical, but can be symmetrical if it is familial.
Numbness does not occur in any of these diseases. Evaluation usually begins with the determination of serum creatikinase levels and electrophysiological studies.
I will complete this post by actually making an introduction to the next one, where I will discuss the dysfunctions of the movement.
Movement dysfunctions are neurological syndromes in which abnormal movements (or dyskinesis) occur due to a disturbance of fluency and speed of voluntary movement or due to the presence of additional unintentional movement. Because they are so distinct from the pyramidal disorders that cause weakness due to the central motor neuron, motion dysfunctions are commonly referred to as extrapyramidal diseases.
Motion dysfunctions are divided into two types, hypokinetic and hyperkinetic. Hypokinetic movement dysfunctions are characterized by akinesis or bradykinesis, in which the proposed motor activity is absent or reduced. This is commonly described as a "poor movement". Hyperkinetic dysfunctions of movement are those in which an excessive amount of spontaneous motor activity is observed or abnormal involuntary movements occur.
Spring
is officially here, so All I can wish for is a spring... And,
a weekend full of understanding, love and gratitude.
Dorin, Merticaru