3.1 week 2 Flashcards
What is neuronopathy?
Neuronopathy refers to damage or dysfunction of the neuronal cell bodies, affecting motor or sensory neurons.
What is radiculopathy?
Radiculopathy is damage or irritation of a nerve root as it exits the spinal column, causing pain, weakness, or sensory loss along the nerve’s distribution.
What is the difference between motor neuronopathy and sensory neuronopathy?
Motor Neuronopathy: Affects motor neurons, leading to muscle weakness and wasting (e.g., ALS).
Sensory Neuronopathy: Affects sensory neurons, causing loss of sensation like numbness or tingling.
What is plexopathy?
Plexopathy is damage or dysfunction of a nerve plexus, a network of intersecting nerves (e.g., brachial or lumbosacral plexus).
What are the symptoms of radiculopathy?
Symptoms include pain radiating along a dermatome, weakness, and sensory loss in muscles innervated by the affected nerve root.
What are common symptoms of plexopathy?
Plexopathy causes motor weakness, sensory loss, and sometimes autonomic dysfunction in areas served by the plexus.
Define neuropathy.
Neuropathy refers to a disorder of the peripheral nerves, affecting motor, sensory, or autonomic functions.
What is the difference between axonal neuropathy and demyelinating neuropathy?
Axonal Neuropathy: The primary damage occurs to the axon, leading to weakness and sensory loss.
Demyelinating Neuropathy: The damage occurs to the myelin sheath, slowing or blocking nerve signal transmission.
What fibers are affected in axonal neuropathy?
Axons, which are the long thread-like parts of the nerve cell that transmit signals, are primarily damaged.
What are common causes of demyelinating neuropathy?
Conditions like Guillain-Barré Syndrome (GBS), where the immune system attacks the myelin sheath around nerves.
What are thick nerve fibers responsible for?
Thick, heavily myelinated fibers carry motor signals, vibration sense, fine touch, and proprioception.
What symptoms arise when thick fibers are damaged?
Damage to thick fibers results in muscle weakness, loss of fine touch, vibration sensation, and difficulty coordinating movements.
What are thin nerve fibers responsible for?
Thin, unmyelinated or lightly myelinated fibers carry sensations like pain, temperature, and crude touch.
What happens when thin fibers are damaged?
Damage to thin fibers leads to loss of pain and temperature sensation and may cause burning or tingling pain.
What is motor neuropathy?
Motor neuropathy affects the motor nerves, causing muscle weakness, atrophy, and possibly paralysis.
What is sensory neuropathy?
Sensory neuropathy affects the sensory nerves, leading to numbness, tingling, burning sensations, or loss of sensation.
What is autonomic neuropathy?
Autonomic neuropathy affects the autonomic nerves, leading to issues with involuntary functions such as blood pressure, digestion, or sweating.
What are exteroceptors?
Receptors that detect stimuli from outside the body (e.g., touch, temperature, pain).
What do interoceptors detect?
Stimuli from within the body, such as internal organ signals and chemical changes.
Name the types of receptors based on what they react to.
Thermoreceptors: Detect temperature changes.
Mechanoreceptors: React to mechanical changes (pressure, vibration).
Photoreceptors: Detect light (in the eyes).
Chemoreceptors: Detect chemical changes (e.g., in taste or blood gases).
What is the role of proprioceptors?
Provide information about the position and movement of body parts, located in muscles, tendons, and joints.
What are nociceptors?
Specialized receptors that detect painful stimuli.
What is an adequate stimulus?
The specific type of stimulus to which a receptor has a low threshold and responds optimally.
Define transduction in the context of sensory receptors.
The process of converting energy from a stimulus into an electrical signal (action potential).
How do receptors interpret sensory information?
Through labeled lines, where specific pathways correspond to specific sensations (e.g., visual or tactile).
What is frequency modulation?
As stimulus strength increases, the frequency of action potentials increases, conveying the intensity of the stimulus.
What is amplitude modulation?
A method where the strength of the receptor potential depends on the amplitude of the stimulus.
How does the intensity of a sensation get determined?
By the strength of activation of individual receptors and the number of activated receptors.
What are tonic receptors?
Receptors that adapt slowly and continue to fire as long as the stimulus is present, providing constant information.
What are phasic receptors?
Receptors that adapt rapidly and stop firing after the initial stimulus, detecting rapid changes.
What is the Dorsal Column-Medial Lemniscus System (DCML) responsible for?
Processing epicritic sensation (fine touch, vibration, proprioception) with high localization.
What is the function of the Anterolateral System (Spinothalamic Pathway)?
Processing protopathic sensation (pain, temperature, crude touch) that lacks high localization.
What are receptive fields?
Areas of skin innervated by a single sensory neuron; smaller fields allow for greater sensory discrimination.
What do muscle spindles measure?
Changes in muscle length and play a key role in proprioception.
What does the sensory homunculus represent?
A topographical map in the cortex showing the representation of body parts based on sensory input.
What is the role of Golgi Tendon Organs (GTOs)?
Measure muscle force at the junction between muscles and tendons, providing protective feedback.
Describe the muscle stretch reflex.
A reflex that causes contraction of a muscle in response to its stretch, helping to maintain posture.
What happens during reciprocal inhibition in muscle reflexes?
While one muscle contracts, the opposing muscle is inhibited to allow smooth movement.
How do Golgi Tendon Organs prevent muscle damage?
They inhibit muscle contraction when excessive force is detected, acting as a negative feedback mechanism.
Which neurotransmitter is released by the muscle spindle
afferents?
a. Acetylcholine
b. GABA
c. Glutamate
d. Noradrenaline
Muscle spindle afferents primarily use glutamate as their neurotransmitter. When muscle spindles are activated (such as during muscle stretch), they send signals to the spinal cord via Ia afferent fibers.
These Ia afferent fibers release glutamate at their synapses in the spinal cord, leading to the activation of alpha motor neurons that innervate the muscle, causing a reflexive contraction.
What sensations are carried by the dorsal column?
Vibration, proprioception, and touch (epicritic).
What sensations are carried by the spinothalamic tract?
Pain and temperature (protopathic).
In the dorsal column, where do fibers cross to the opposite side?
At the medulla oblongata.
What is the significance of a positive Romberg test?
Indicates sensory ataxia, showing proprioception issues.
In the spinothalamic tract, where do fibers cross to the opposite side?
At the level of entry in the spinal cord.
What are the main clinical signs of dorsal column dysfunction?
Loss of vibration, position sense, and proprioception.
What does a bilateral Babinski sign suggest?
Upper motor neuron (UMN) lesion, typically in the pyramidal tracts.
What are the key findings in subacute combined degeneration?
Loss of dorsal column function (sensory) and pyramidal tract dysfunction (motor).
What can cause subacute combined degeneration (SCD) of the spinal cord?
Vitamin B12 deficiency, often linked to nitrous oxide abuse.
In Brown-Séquard syndrome, what sensory loss occurs ipsilaterally and contralaterally?
Ipsilateral: Loss of epicritic sensation and motor function below the lesion.
Contralateral: Loss of protopathic sensation below the lesion.
What characterizes central cord syndrome?
Greater motor impairment in the arms than the legs, with sacral sparing.
What symptoms are typical of cauda equina syndrome?
Lower limb weakness, bladder/bowel dysfunction, and saddle anesthesia but no Babinski sign.
What is the main cause of anterior spinal artery syndrome?
Infarction of the anterior spinal artery, leading to loss of motor function and protopathic sensation, with spared epicritic sensation.
What is a common neurological effect of nitrous oxide abuse?
Vitamin B12 deficiency, leading to subacute combined degeneration (SCD) of the spinal cord.
Which spinal cord syndrome is associated with sacral sparing?
Central cord syndrome.
What are the main non-traumatic causes of spinal cord injury?
Compression (tumor, herniation), metabolic (e.g., B12 deficiency), vascular (infarction), inflammatory (MS, myelitis), degenerative, and intoxication (e.g., nitrous oxide).
In which spinal cord syndrome would you find “man in a barrel” syndrome?
Central cord syndrome.
What distinguishes a sensory ataxia from a cerebellar ataxia?
Sensory ataxia worsens when eyes are closed (Romberg test positive), while cerebellar ataxia affects balance even with eyes open.
What are the effects of pyramidal tract dysfunction in the spinal cord?
Loss of voluntary motor control, usually affecting proximal muscles.
What are the signs of a complete spinal cord injury?
Paralysis and loss of sensation below the injury, often with neurogenic and spinal shock.
What are the key symptoms of cervical spinal cord compression in a 60-year-old man?
Balance problems, stiff gait, urinary urgency/incontinence, difficulty buttoning shirts, and mixed sensory and motor dysfunction.
What does difficulty walking in the dark suggest in a neurological exam?
Sensory ataxia due to loss of proprioception, likely from dorsal column dysfunction.
What findings on neurological examination suggest cervical spinal cord compression?
Decreased epicritic sensation in legs and arms, brisk reflexes in legs, low or absent reflexes in arms, Babinski sign.
What is the significance of a stiff gait in this patient?
It suggests hypertonia and pyramidal tract involvement, indicating a CNS problem.
What differential diagnosis should be considered in a patient with balance problems and sensory/motor dysfunction?
Cervical spinal cord compression, distal symmetric polyneuropathy, and cervical myelopathy.
What diagnostic test is essential for confirming cervical spinal cord compression?
MRI of the cervical spine to visualize compression and degenerative changes.
What is the typical presentation of cervical spinal cord compression?
Slow progression with mixed UMN and LMN signs, sensory loss, stiff gait, and urinary incontinence.
What does the combination of increased reflexes in the legs and reduced reflexes in the arms suggest?
Cervical spinal cord compression, where UMN signs are present in the legs and LMN signs are present in the arms.
Why should Vitamin B12 levels be checked in a patient with suspected cervical myelopathy?
To rule out subacute combined degeneration (B12 deficiency), which can mimic myelopathy.
What are the possible causes of cervical spinal cord compression?
Degenerative changes such as disc herniation, osteophytes, and ligament hypertrophy.
What is the effect of cervical spinal cord compression on sensory and motor pathways?
It affects the pyramidal tracts (causing spasticity) and dorsal columns (causing loss of proprioception and vibration).
What is the prognosis for untreated cervical myelopathy?
It can lead to significant disability, including paralysis, if left untreated.
What is the typical patient profile for cervical spondylotic myelopathy?
Patients over 60, with slowly progressive symptoms of motor and sensory dysfunction, sometimes worsened after a fall.
What is the preferred surgical treatment for cervical spinal cord compression?
Anterior cervical discectomy and fusion (ACDF) or posterior laminectomy to decompress the spinal cord.
How does cervical spinal cord compression affect bladder function?
It can cause urinary urgency and incontinence, due to involvement of central pathways controlling the bladder.
Which symptoms distinguish cervical spinal cord compression from polyneuropathy?
UMN signs like Babinski reflex and hyperreflexia in the legs, which are absent in polyneuropathy.
What are the expected MRI findings in cervical spondylotic myelopathy?
Spinal cord compression due to degenerative changes such as disc herniation or osteophytes.
What is the risk of delaying treatment for cervical spinal cord compression?
Delay in treatment increases the risk of permanent motor and sensory deficits, including paralysis.
What is the impact of cervical spinal cord compression on reflexes in the arms?
It causes reduced or absent reflexes in the arms due to nerve root compression (LMN involvement).
What is the key clinical feature of spastic gait in cervical myelopathy?
Stiffness and hypertonia due to pyramidal tract dysfunction.
Why might a patient with cervical myelopathy have difficulty buttoning a shirt?
Due to fine motor control issues from sensory loss and possible weakness in the hands.
What conditions can mimic cervical spinal cord compression?
Subacute combined degeneration (B12 deficiency), multiple sclerosis, and syringomyelia.
What is the typical progression of symptoms in untreated cervical spinal cord compression?
Gradual worsening of motor and sensory function, possibly leading to severe disability or paralysis.
What surgical outcomes can be expected in cervical myelopathy?
Early surgery can improve or stabilize symptoms, while delayed surgery may result in persistent deficits.
