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369 Cards in this Set

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The primary motor pathway is comprised of two central components. What are they?
Upper motor neurons
Lower motor neurons
Where do upper motor neurons project to and from?
Project from cortex to spinal cord.
Where do lower motor neurons project?
Lower motor neurons project from the spinal cord to muscle.
The cell bodies in the motor cortex project their axons through the internal capsule in the corticospinal tract. TRUE/FALSE
TRUE. This is the main motor pathway.
How do the cell bodies in the motor cortex fibers descend?
They descend in the brainstem, cross(decussate) in the lower medulla(medullary pyramids, and then descend as the lateral corticospinal tracts in the spinal cord.
These corticospinal tract fibers from the cortex to the spinal cord are called what?
Upper motor neurons. (UMN)
Where do the upper motor neurons synapse?
On the anterior horn cells in the anterior spinal cord.
The anterior horn cells and their axonal projections in peripheral nerves are called lower motor neurons. TRUE/ FALSE
TRUE. The anterior horn cells and their axonal projections in peripheral nerves are called lower motor neurons
Where do lower motor neurons synapse?
Lower motor neurons synapse on muscles.
Due to the decussation of the corticospinal tract in the medulla, the right motor cortex controls what?
The left side of the body. The left cortex controls the right side.
What might result if there is a lesion anywhere in the motor pathway?
The result will be weakness or aesthenia of the affected muscles. However, UMN or LMN defects will have different symptoms.
What are some typical symptoms of LMN disease?
Flaccid paralysis, diminished reflexes, fasciculations and eventual muscle atrophy.
How might one explain or justify LMN symptoms?
If there is an injury of anterior horn cells, and or peripheral nerve cells, where axons travel, the signals are not likely to arrive.
How might one explain spasm or tonic contraction in UMN disease?
If there is a lesion anywhere in the UMN pathway, including the internal capsule, medulla or spinal cord, lower motor neurons fire spontaneously causing spasm. There is a loss of inhibition from above. Reflexes become exaggerated or hyperactive.
What is Babinsky's sign?
If you stroke the bottom of the foot, the toes should normally curve down. Should the big toe go up, this is the Babinsky sign and is abnormal in adults. It can indicate a lesion anywhere in the UMN pathway.
How is Babinsky's sign, demonstrated in LMN disease?
Babinsky's sign is not seen in LMN diseases.
Why is Babinsky's sign considered normal in newborns?
Myelination is not yet complete. The big toe will go up with this test.
What is Clonus?
It is a repetitive, rhythmic contraction of a muscle when it is stretched, often seen in the ankle.
Clonus is another example of disinhibition. TRUE/FALSE
TRUE. Clonus is another example of disinhibition
If the lesion is above the decussation of the corticospinal tract, in the medullary pyramids, where will the motor deficit be?
On the contralateral(opposite) side of the body from the lesion.
Where would the lesion be if the motor deficit is on the ipsalateral side(same)?
The lesion would be below the decussation if the motor deficit is on the ipsalateral side(same)
What are the two main sensory pathways?
The posterior columns(dorsal)
The spinalthalamic tracts(anterolateral tracts).
What do the posterior columns transmit?
Discriminative touch, vibration and positional sense.
The spinothalamic tract carries what type of sensation?
Pain and temperature sensation.
All of the sensory input comes from where?
The periphery(skin, muscle spindle via peripheral nerves) that enter the cord posteriorly.
Do the spinothalamic pathways cross immediately in the cord?
Yes. They form the spinothalamic tracts.
Where do the posterior columns go?
They stay ipsilateral until the brainstem, and then cross in the medulla, continuing as the medial lemnisci(which project to the thalamus)
If there were a lesion of the posterior column on the left side at about the level of the umbilicus, where might there be a deficit?
Since the sensory information has come from that same side, and stays on that side until the brainstem, one might lose discriminative touch/vibration, position sense on the same side, distal to the lesion.
What about a lesion of the spinal thalamic tract on the left side?
Since those fibers came from the right side, a lesion of the spinothalamic tract on the left would lead to loss of pain and temperature sensation below the lesion on the contralateral side, in this case on the right side.
In the spinothalamic tract, first order sensory neurons synapse where?
Immediately upon arrival in the cord. Second order neurons cross and ascend as the spinothalamic tract.
Where do most of the axons of the first order in the posterior columns travel?
All the way to the medulla, where they synapse onto neurons that cross there and ascend to the thalamus as the medial lemniscus.
Ipsilateral lesions of the spinal cord often do not result in much loss of light touch. TRUE/FALSE
TRUE. Some light touch sensation is preserved in fibers that cross.
What if a lesion destroyed the entire left half of the cord?(Brown-Sequard syndrome)
Only the spinothalamic tract(pain and temperature) crosses in the spinal cord.
Paralysis and discrimination/vibration sense/proprioception loss will occur on the same side of the body below the level of the lesion, whereas loss of pain and temperature will occur on the contralateral side of the body below the level of the lesion.
If strength, light touch, pain, temperature, sensation, is lost on only one side of the body, with the other side normal, could this be due to spinal cord injury?
Not really.A spinal cord lesion would typically have some contralateral effect because of the crossing of the spinothalamic tract. Loss of everything on only one side must localize to somewhere to outside of the cord.
Give an example for the following explanation. If strength, light touch, pain, temperature, sensation, is lost on only one side of the body, with the other side normal, could this be due to spinal cord injury?
A middle cerebral artery stroke can cause ischemia/ infarction of both the motor cortex and the sensory cortex on one side, leading to contralateral hemiparesis and sensory loss.
Is it true that a peripheral nerve lesion could also lead to loss of motor and sensory function together on one side?
Yes, but the effects would not be total. It would have to be in a region limited to the distribution of the nerve.
Compression of sensory(posterior/dorsal) nerve roots as they enter the spinal cord leads to symptoms confined to specific dermatomes. TRUE/FALSE
TRUE. Dermatomal sensory deficits only occur with focal cord lesions or nerve root compression.
Can it be said that the cortex is the starting point of the motor system?
Yes. The cortex also represents the end of the sensory system. This is where ascending sensory input from the body finally arrives.
Do the motor and sensory pathways run very close to each other?
Yes. The motor and sensory pathways run very close to each other. They do run however separately through the brainstem and spinal cord. They exit as well as separate as anterior(ventral) motor and posterior(dorsal)sensory roots respectively.
In the CNS, isolated motor or sensory deficits may typically occur with small isolated lesions in very specific places. Give an example of this.
A lacunar infarct, which is an occlusion of a smallpenetrating vessel in the brain.
Can small lacunar infarcts lead to a stroke?
Lacunar infarcts can lead to strokes with only motor deficits or only sensory deficits.
In the PNS, causes of isolated motor or sensory deficits include what type of lesions?
Root lesions or diseases affecting the motor or sensory systems specifically.
Prolapsed discs or tumors that compress only the anterior(ventral) or posterior(dorsal) roots may also lead to isolated motor or sensory findings. TRUE/FALSE
TRUE. This is because the motor and sensory fibers are relatively separate in the spinal cord and spinal roots. They tend to be mixed in peripheral nerves.
This structure contains most of the cranial nerve nuclei, connections with the cerebellum, and the descending motor and ascending sensory pathways. What is it?
The brainstem.
What three divisions make up the brainstem?
An approximate way to remember where the cranial nerves exit/enter is:
1-1V are in the midbrain, V-V111 are in the pons, and 1X-X11 are in the medulla. Is this an accurate statement?
It is somewhat accurate. There are near exceptions to this rule, that involve CNN 1, 11,V, and V111.
Explain the exception of CN 1 with regard to where it is located.
The olfactory nerve does not project to the brainstem at all but to the olfactory cortex.
Explain the exception of CN 11 with regard to where it is located.
The optic nerve does have fibers that project to the midbrain(pretectal nucleus) for the afferent limb for the pupillary light reflex, but the visual pathway carried in cranial nerve 2 does not project to the brainstem,
Where do the visual pathway fibers in cranial nerve 2 project to?
To the lateral geniculate nucleus of the thalamus.
The spinal trigeminal nucleus, receives facial sensation information from cranial nerve V. TRUE/FALSE
TRUE. However, the trigeminal nerve spans much of the brainstem and extends into the upper spinal cord.
The vestibular nuclei of CN V111(vestibularcochlear nerve) situate themselves on this important junction found in the brainstem.
The Ponto-medullary junction.
How do the cranial nerves generally exit the brainstem?
In an anterior direction and they project themselves ipsilaterally.
Do all the cranial nerves exit the brainstem in the same fashion?
No. The trochlear nerve(1V) exits the brainstem posteriorly and projects itself to the contralateral superior oblique muscle.
It is not until the medullary pyramids(the bottom of the medulla) that motor fibers in the corticospinal tract cross to the other side. Is this statement accurate?
Consider the following scenario: If there is a brainstem lesion above this crossing over(decussation) in the medulla, it will impair motor and sensory function on the opposite side of the body, but cranial nerve function will be impaired on the same side.
Is this statement true, and if so, why?
It is true. Cranial nerve function will be impaired on the same side because the cranial nerves project ipsilaterally.
If cranial nerve function is lessened on the left with paralysis and/or sensory loss on the right side of the body, below the head, this might indicate a brainstem lesion on which side?
The left.
If cranial nerve function and paralysis and/or sensory loss below the head are on the same side, this generally implies a lesion where?
Above the brainstem, such as the cerebral cortex, internal capsule and thalamus.
The olfactory nerve transmits smell information from which two major structures?
The olfactory nerve transmits smell information from the nose to the brain.
What is anosmia?
It is the loss of smell. A lesion of the first cranial nerve leads to this condition.
What is the most common cause of the loss of smell?
The most common cause of anosmia is nasal obstruction, such as a cold or sinusitis.
What are some other organic causes of anosmia?
Some other organic causes of anosmia are aging, trauma,(skull fracture,
Kallman's syndrome(loss of olfactory neurons, loss of GnRH secreting cells resulting in hypogonadism or a tumor(meningioma) impinging on the olfactory nerve.
Would a tumor, such as a meningioma or a frontal lobe mass be more likely to cause unilateral or a bilateral anosmia?
A meningioma or frontal mass would likely cause a unilateral loss of smaell, as it would be placing pressure on one side of CN 1.
How does CN 1 connect to the brainstem?
CN1 does not at all connect to the brainstem. It projects to the temporal lobe olfactory area.
CN 2, the optic nerve convey's visual information from the eyes to the......
CN 2, the optic nerve convey's visual information from the eyes to the brain for visual processing.
A lesion of CN2 can lead to what?
A lesion of CN 2 can lead to blindness, either in part or total blindness in one or both eyes.
CN 2 is also the afferent sensory limb of what important reflex?
CN 2 is also the afferent sensory limb of the pupillary light reflex.
CN 2 also sends minor projections to the suprachiasmatic nucleus of the hypothalamus(circadian rhythm). TRUE/FALSE
TRUE. Projections are also sent to the superior colliculus. These may involve eye-head orienting reflexes.
Light hits the retina, which eventually converts that information into what?
The retina eventually converts the light source into electrical activity.
Once the impulses are traveling in the optic nerves, half of these axons cross at the optic chiasma. TRUE/FALSE
After the optic chiasma these axons are now known as the ______________ tracts.
Optic. After the optic chiasma these axons are now known as the optic tracts.
Where do the optic tracts synapse?
The optic tracts synapse at the lateral geniculate nuclei of the thalamus.
What is Meyer's loop?
After the synapse in the thalamus, there are 2 projections(on each side), one going in a superior pattern and one going inferiorly. This is Meyer's loop.
After Meyer's loop, these pathways will synapse where?
These axons will synapse in the occipital lobe.
Regarding the retinal activation, after light has entered the eye, does all light always hit on the same retinal area?
How light enters the eye, and from which direction is a key characteristic. Looking directly ahead, and if a beam of light coming from the right, the beam will impinge on the left portion of both retinas.
A beam from the top, will hit the bottom of the retinas. One from the bottom will hit the top. This is the general pattern.
The left brain contains information about the right visual field, and the right brain will concern the left visual field. TRUE/FALSE
This statement is true. Light originating from the left taps into the right brain, and from the right into the left brain.
Regarding a lesion of the optic chiasm at the midline, can it be said that information from the lateral parts of both retinas still makes it to the brain.
This is a true statement.
Regarding a lesion of the optic chiasm at the midline, information from the lateral parts of both retinas still make it to the brain.
Considering the optic chiasm lesion at the midline, from the right eye, this is the left visual(nasal)field, and from the left eye this represents the right(nasal) visual field. TRUE/FALSE
TRUE.Considering the optic chiasm lesion at the midline, from the right eye, this is the left visual(nasal)field, and from the left eye this represents the right(nasal) visual field.
What is lost is the information that crosses from the medial parts of the retinas: the left visual temporal field of the left eye and the right temporal visual field of the right eye. So the result is the loss of lateral temporal visual fields on both sides due to the outer visual fields hitting the inner retinas.
What is bitemporal hemianopsia?
Loss of the lateral visual fields on both sides, because the outer visual fields hit the inner retinas.
What could be a cause of bitemporal hemianopsia?
Pituitary tumors.The pituitary lies beneath the optic chiasm and it could press on the chiasm at the midline.
Regarding a lesion of the optic tract, a postchiasmatic lesion of one optic tract leads to a loss of what?
A postchiasmatic lesion of one optic tract leads to a loss of the entire contralateral visual field.
The optic tracts carry all iformation from the contralateral visual field(lateral retinal fibers from the ipsilateral eye and the crossed medial retinal fibers from the contralateral eye. Does this stsement sound accurate?
Yes. The optic tracts carry all iformation from the contralateral visual field(lateral retinal fibers from the ipsilateral eye and the crossed medial retinal fibers from the contralateral eye.
Consider the established statement: "Maintaining the opposites pattern, lower visual field information travels in the upper loop, and upper visual field travels in the lower loop".
What type of visual defect or deficit would a left Meyer's loop lesion cause?
A left Meyer's loop lesion would cause a loss of the right upper visual field, also referred to as a right upper quadrantanopsia or a " pie in the sky" lesion. Therefore an upper loop lesion leads to a contralateral lower quadrantanopsia.
A lesion of the entire occipital cortex on one side leads to a complete loss of what?
A lesion of the entire occipital cortex on one side leads to a complete loss of the contralateral visual field(homonymous hemianopsia).
Because the center of the visual field that corresponds to the macula or the retina, is the most important, it receives dual blood supply from which two cerebral arteries?
The center of the visual field that corresponds to the macula or the retina, is the most important. It receives dual blood supply from the middle and posterior cerebral arteries.
Can visual loss also be caused by non neurological diseases of the eye?
Non neurological diseases of the eye can be caused by retinal diseases, cataract formation, or age related changes to the eye.
Visual field deficits such as hemianopsia, quadrantanopsia, indicate a lesion of the visual pathway. TRUE/FALSE
TRUE. Visual field deficits such as hemianopsia, quadrantanopsia, indicate a lesions of the visual pathway, i.e. optic nerve, tracts, radiations or occipital cortex.
Opthalmic examinations can reveal organic eye disease.
Refractive errors such as nearsightedness(myopia), far-sightedness(hyperopia), age related accomadation/focusing difficulty(presbyopia) will improve if the patient reads through a pinhole or with corrective lenses. Is this statement true. If not, correct.
This statement is true.
What type of lenses are employed for myopia and hyperopia?
For myopia concave lenses are used. For hyperopia and presbyopia, concave lenses are used.
Which 4 extraocular muscles does CN3 innervate?
The inferior oblique and the superior, inferior and medial rectus muscles.
Does the third CN have an affect on the eyelids?
The third CN innervates the levator palpebrae muscle which raises the eyelid.
CN 3 also provides parasympathetic innervation to the pupil. TRUE/FALSE
TRUE. CN3 also provides parasympathetic innervation to the pupil.
How is parasympathetic ocular constriction mediated?
Parasympathetic ocular constriction is mediated by fibers traveling within CN 3.
A lesion of CN3 would weaken which muscles?
A lesion of CN 3 would weaken all eye muscles on that side with the exception of the superior oblique which intorts and depresses the eye which is innervated by CN 1V, and the lateral rectus which abducts the eye, innervated by CN 1V.
If a lesion results in the non functioning of the inferior oblique, as well as the superior, inferior and medial rectus muscles, how will the eye appear?
The superior oblique and the lateral rectus muscles are unopposed and will pull the eye down and out.
Considering that the levator palpebrae muscles and pupillary constrictors are lost due to a CN 3 lesion, how will the eye appear?
The result is a dilated pupil and a drooping eyelid(ptosis).
What type of lesions can negatively affect the third cranial nerve?
Aneurysms, tumors, infectious or inflammatory processes and vascular injury can all result in CN 3 loss.
What is the response when light is shone into the eye?
When light shines into the eye, the pupil normally constricts in response. This is accomplished by the optic nerve(afferent) and the oculomotor(efferent).
If the ocular optic pathway is intact bilaterally, shining light into either eye will cause constriction of both pupils. TRUE/FALSE
TRUE. If the ocular optic pathway is intact bilaterally, shining light into either eye will cause constriction of both pupils. This is true because the efferent signal is sent via both oculomotor nerves to both pupils in order to cause a symmetrical pupillary response.
Regarding pupillary constriction, what is the difference between direct and consensual response?
Pupillary constriction as it responds to light in the ipsilateral eye is direct response.Constriction on the opposite or contralateral eye is referred to as consensual.
A right CN 111 lesion would prevent the right eye from constricting in response to light in either eye. Under such circumstances, is it still possible to get a left pupil constriction?
Yes. If CN 11 is still functioning, on the right, light shined in the right eye can still be transmittted through this afferent pathway and result in constriction of the left pupil.
What other circumstance might cause physiological variability in pupil constriction?
Pupils do not respond only to light, but also as part of accommodation for the focusing on approximate objects.
What are Argyll- Robertson pupils?
Argyll-Robertson pupils are often seen with syphilis. Although the light and near responses are usually lost together, A-R pupils constrict in accommodation but do not react to light.
Define " Adie's pupil".
Adie's pupil is a dilated pupil that constricts gradually when exposed to light. It does respond more physiologically during accommodation.
What can cause Adie's pupil?
Adie's pupil may be the result of ciliary ganglion damage. This branch importantly contains parasympathetic input from CN111 that is responsible for constricting the pupil.
Define Holmes-Adie syndrome.
Holmes-Adie syndrome involves Adie's pupil with the absence of deep tendon reflexes(leg and ankle) and orthostatic hypotension or other autonomic dysfunction. This condition is more common in younger women.
What is meant by the "triad of Horners syndrome?
The triad of Horner's syndrome involves:
1. Ptosis-drooping eyelid
2.-Miosis-constricted pupil
3.Anhydrosis-loss of sweating.
What might specifically and anatomically(lesional) cause Horner's syndrome?
There may a lesion in the sympathetic pathway in some place along its path from itd origen in the hypothalamus down to the cervical spinal cord to the superior cervical ganglion back up to the face and eyes.`
List three major causal possibilities of Horner's syndrome.
Lateral brainstem infarcts
Spinal cord lesions
Apical pulmonary tumors.
The ptosis in Horner's syndrome results in loss of which autonomic deficit?
The ptosis results from loss of sympathetic input to the tarsal muscles, which retract the eyelids.
Define anisocoria.
Pupillary asymmetry is anisocoria. Some drugs administered unilaterally may have this effect. Certain nerve tract lesions may as well have this effect.
What does CN1V innervate?
CN1V innervates the superior oblique muscle
The superior oblique muscle can can intort and depress the eye. TRUE/FALSE
TRUE. It stands to reason that a lesion of CN1V might reduce the ability to intort and depress the eye, which would result in ocular extortion and weakness of the downward gaze, especially in ocular adduction(turned medially).
When there are losses of rotary functions what might be seen as a compensating action?
With losses of rotary functions, intorting and extorting, a head tilt might be seen as a compensatory reaction.
CN V has both sensory and motor function. TRUE/FALSE
TRUE. The trigeminal nerve has both motor and sensory function.
Briefly define the sensory function of CN V.
Facial sensation: skin, sinuses, tongue(not taste) just sensation and corneal sensation. Some trigeminal function involves as well the tympanic membrane and part of the meninges.
Describe some motor functions of the trigeminal nerve.
Innervation of chewing muscles.
There is some innervation of the tensor veli palitini muscle, found in the soft palate.
What are the three branches of CN V that deliver sensory information to the brain from the face?
The three branches of CN V that deliver sensory information to the brain from the face are the opthalmic, maxillary and mandibular.
If there is sensory loss localized to only one of the facial regions, what might this imply?
This would imply or suggest a lesion between the face and the trigeminal ganglion from which the branches emerge.
Is CN V considered the afferent(sensory) limb of the corneal reflex?
CN V is indeed considered the afferent(sensory) limb of the corneal reflex. A blink of the eyelid in response to stimulation of the cornea would be an example.
This blink reflex may be absent in a CN V lesion. A lesion in CN V11 may result in lack of blink reflex as well.
What does the Abducens nerve innervate?
The Abducens nerve innervates the lateral rectus, which abducts the eye.
What might be the result of a lesion of CN V1?
A lesion of CN V1 leads to an ipsilateral inability to abduct the eye.
What is the Conjugate Gaze Pathway?
When one looks to the left, both eyes must move to the left in a controlled synchronized fashion.
Which muscles and nerves are responsible for the Conjugate Gaze Pathway?
Looking to the left, the left eye abducts and the right adducts. The left lateral rectus, which is innervated by the left abducens nerve(V1), abducts the eye(lateral). The right medial rectus, innervated by the right oculomotor nerve(111), adducts the right eye(medial).
How is the abduction and adduction process of both eyes mediated?
The medial longitudinal fasciculus(MLF) in the brainstem allows for communication between the nucleus of V1(in the pons) and the contralateral nucleus of CN111(midbrain).
Why is the reaction of the MLF considered contralateral?
It is contralateral because the MLF coordinates abduction in one eye with adduction in the contralateral eye.
What is Internuclear opthalmoplegia?(INO)
A lesion of the MLF results in INO, in which the eye ipsilateral to the lesion cannot adduct during attempted conjugate gaze. The side of the lesion is named for the side of the medial rectus dysfunction, which is the same side as the MLF, after it has crossed to the side of the affeced CN 111 nucleus.
Give an example of a right MLF lesion.
A lesion of the right MLF means that the left abducens(V1) nucleus in the pons cannot communicate with the right oculomotor(111) nucleus in the midbrain.
Patients looking to the left, the left eye will abduct but the right eye cannot adduct.
What are some common causes of INO?
Common causes of INO are brainstem strokes and Multiple Sclerosis. Bilateral MLF lesions are possible.
List 5 functions of CN V11.
1. Innervation of facial musculature and stapedius muscle of inner ear.
2. Taste sensation of 2/3 anterior portion of tongue.
3. Salivary gland stimulation
4. Lacrimal gland stimulation
5. Sensations from parts of the inner ear.
Which salivary glands are stimulated by the facial nerve?
Submaxillary and submandibular are stimulated by the facial nerve.
The parotid is controlled by CN 1X.
The facial nerve on each side receives contralateral input for the forehead and lower face in addition to ipsilateral cortical input for the forehead. Is this an accurate statement?
This is an accurate statement.
The facial nerve on each side receives contralateral input for the forehead and lower face in addition to ipsilateral cortical input for the forehead. Is this an accurate statement?
Can unilateral cortical lesions concerning the facial nerve involve the forehead muscles?
NO. Since innervation to the forehead comes to the facial nerve from both sides of the brain, unilateral cortical lesions can affect the muscles of the lower face, while sparing the forehead.
A lesion of the facial nerve(CN V11) will cause weakness of the muscles of the whole face, forehead included on that same side. TRUE/FALSE
TRUE. A lesion of the facial nerve(CN V11) will cause weakness of the muscles of the whole face, forehead included on that same side.
What are some causes of facial nerve palsy?
Facial nerve palsy causes include: Infectious diseases(Herpes Zoster, HIV, Lyme disease), Multiple sclerosis, Sacoidosis and tumors compressing on the seventh cranial nerve, such as acustic neuroma.
What is Bell's palsy?
This is an idiopathic form of palsy of CN V11.
A patient with an UMN lesion(cortical stroke) will have loss of contralateral lower face movements but normal forehead movements. TRUE/FALSE
TRUE. This is so because the facial nerve is still carrying input to the forehead from ipsilateral cortex.
What does CN V111 do?
The vestibularcochlear nerve, conveys sound as well as head movement(positional information) to the brainstem from the cochlea and semicircular canals.
Give an example of a lesion that may affect the CN V111.
An acoustic neuroma(vestibular schwannoma). These CN V111 tumors may lead to unilateral hearing loss and vestibular deficits.
What are some non-neurological causes of hearing loss?
Middle ear infections with/without congestion, damage to the tympanic membrane, ossicles or cochlea, and less frequently cholesteotomas.
What are some non-neurological causes of dizziness and balance problems?
Sytemic diseases(cardiovascular disease, anemia and inner ear diseases, such as benign paroxysmal positional vertigo and Meniere's disease. Advanced forms of cholesteotomas may as well result in sensations of dizzyness. Post-surgical effects such as dizzyness may exist or occur temporarily for the removal of inner or middle ear lesions.
What is the vestibulo-ocular reflex?
This keeps vision steady while the head is moved by causing the eyes to move in the opposite direction from the head as the head turns, as long as the eyes are not following a moving object.
Describe briefly how the vestibular ocular reflex system works.
The VOR reflex is rather complex. The brainstem gets information from CN V111 and transmits it to the relevant eye movement nuclei(CN 111, 1V, and CN V1) generating the appropriate eye movements.
What is the doll's eye test in a comatose patient?
This test(doll's eye test) tests the integrity of the VOR system. If the head is turned in one direction , the eyes move in the opposite direction, this indicates that the brainstem is intact. Should the eyes move in the same direction as the head, this implies that the VOR is not functioning normally, and a brainstem lesion may be present.
When should a doll's eye test not be performed?
If spinal or cervical injury is suspected.
What is Nystagmus?
Nystagmus is the oscillation of the eyes, such as the starring at passing telephone poles out the window of a moving train.
Describe Nystagmus more specifically.
The eyes repetitively slowly to one side and then move in the opposite direction rapidly.
The direction of the Nystagmus is named for the "fast phase"(flicking back rapidly).
Can Nystagmus occur physiologically?
It may occur normally at extreme gazing, but is usually due to some pathological nature.
What type of lesions may result in Nystagmus?
Lesions of the vestibular peripheral system, brainstem or cerebellum. Certain drugs mayt cause Nystagmus.
Drugs like Dilantin, Cerebyx, Phenytoin, Phenobarbital(seizures) Peganone(anticonvulsant) etc.
What is " cold caloric testing"?
Putting cold water into one ear mimics a temporary lesion of the vestibular system on that side.
In normal patients, this causes the eyes to move slowly toward the cold side, followed by a quick return in the opposite direction.
This tests the integrity of the vestibular V111/V1/MLF/111 system.
What is the significance of lack of response to the cold water assessment?
This may result as a sign of drug intoxication. There may be as well, a lesion anywhere along this pathway, or tere may be too much wax in the ear to adequately perform the test. An intact tympanic membrane should always be observed prior to performing this test,
List several functions of the ninth cranial nerve.
1. Sensation and taste from the rear third of the tongue and sensory input from the palate.
2. Motor input to the stylopharyngeus muscle of the pharynx.
3. Parotid gland activation.
4. Visceral sensory information transmission from the carotid sinus(volume) receptors to the nucleus solitarius of the medulla.
Sensation from a part of the external ear and tympanic membrane involves the glossopharyngeal nerve. TRUE/FALSE
TRUE. Sensation from a part of the external ear and tympanic membrane involves the glossopharyngeal nerve.
Describe the complimentary relationship between CN V11 and 1X.
This is true with regard to taste(anterior 2/3 of the tongue=CN V11, posterior 1/3=CN 1X, and salivation(submandibular and submaxillary glands=CN V11, parotid gland= CN 1X.
Can a lesion of CN 1X lead to an absence of the gag reflex?
Yes. A lesion of CN 1X can lead to an absence of the gag reflex.
What part of the autonomic nervous system should one think of when the "vagus" nerve is mentioned?
The parasympathetic system.
What does the vagus nerve supply?
It supplies the parasympathetic input to the heart, lungs and most of the GI system.
The bladder, descending colon, rectum and genitals receive their parasympathetic input from the sacral spinal cord.
Does the vagus carry any sensory information?
Yes. It carries sensory information to the brainstem from the viscera and the aortic arch(O2 tension and blood volume information).
Does the vagus provide any notor input?
The vagus nerve provides motor input to one muscle of the tongue(palatoglossus) and all muscles of the larynx and pharynx except the stylopharyngeus muscle (CN 1X) and tensor veli palatini muscle(CN V).
What is the vagal test for palate deviation?
When a patient opens his mouth and says ahhh, one is checking the vagus nerve. Should the uvula elevate symmetrically in the midline, both sides of the pharynx are pulling it simultaneously. Should the uvula deviate to the left, this may signify that the right side vagal structure is weak.
A lesion of the right vagus nerve allows the left side to predominate with the so called pulling, and the uvula deviates to the normal side.
What are some symptoms of vagal nerve damage?
Hoarseness may occur as a result of loss of the laryngeal muscle innervation. Trouble swallowing and loss of the gag reflex are other possible suggestive symptoms.
Where does the recurrent laryngeal nerve come from?
It is a branch of the vagus. It can be compressed by a tumor or damaged in neck surgery(thyroid).
Hoarseness is a result of recurrent laryngeal nerve lesions.
What does CN X1 innervate?
The spinal accessory nerve innervates the sternocleidomastoid and trapezius muscles.
Is there a way to test for the proper function of CN X1?
Yes.When a patient is asked to shrug against resistance or to turn his head against hand resistance, testing for strength, you are assessing CN X1.
Could a lower motor neuron lesion lead to shoulder drop?
Yes. It could result in weakened shrugging as well as weakness turning te head against resistance, toward the opposite side, due to the fact that the sternocleidomastoid muscle normally rotates the head to the opposite side.
What does CN X11 innervate?
The hypoglossal nerve innervates the musculature of the tongue(except the palatoglossus, which is actually innervated by CN X.
What is the justification for tongue protrusion testing?
It is important to remember that the tongue muscles on each side push the tongue to the opposite side. When they work perfectly together, the tongue will protrude straight out. The movement represents an average muscular vector force.
What can be inferred if the tongue protrudes to one side?
If one side has a lesion, the other side will push the tongue toward the weakened side.
If the lesion affects the lower motor neurons the weak side is ipsilateral to the lesion. TRUE/FALSE
TRUE.If the lesion affects the UMNs(from the cortex down to but not including the nucleus in the medulla, the weak side is contralateral to the lesion.
What is the relationship between the cerebellum and the spinal cerebellar tracts?
The cerebellum uses feedback from the spinocerebellar tracts(which tend to travel uncrossed from the spinal cord to monitor movements while they are occurring.
Output to ther cerebral cortex by way of the thalamus is used to adjust these movements.
What else is the cerebellum involved in generally?
The cerebellum is also involved in balance and posture.
Logically, cerebellar lesions will result in what?
Cerebellar lesions may result in ataxia(uncoordinated movement). Movements such as finger to nose may be difficult.
What is dysdiadochokinesia?
Dysdiadochokinesia is the inability to perform rapid alternating movements. Cerebellar lesions may demonstrate this condition.
Define intention tremor.
This is a tremor that is non-existant at rest, but becomes noticeable when the patient has intention to move an object or handle something small. Holding a fork, or picking up a spoon may be examples.
Where do cerebellar deficits occur with respect to the lesion?
Cerebellar deficits occur ipsilateral to the side in which the lesion occurs.
What can cause cerebellar dysfunction?
Cerebellar dysfunction may be caused by certain toxins, such as alcohol. multiple sclerosis, tumors or paraneoplastic syndromes.
What are the substructures of the basal ganglia that are part of the loop circuit that begins and ends in the cortex?
Basal ganglia substructures include:
Subthalamic nucleus
Nucleus Acumbens
Globus Pallidus
Substantia nigra.
Lesions of the basal ganglia tend to cause what type of movement?
Basal ganglia lesions tend to cause unwanted movements at rest. The resting tremor of Parkinson's disease is an example.
What might be some other examples of syndromes or diseases seen with basal ganglia lesions?
Dystonia-painful muscular contraction resulting in undesired and unusual postures.
Hemiballismus-violent and unilateral involuntary movements resulting from contralateral lesion of the subthalamic nucleus.
Chorea-involuntary dance like movements.
Huntingtons disease(autosomal dominant inherited degeneration of the caudate putamen.
Sydenhams chorea-chorea seen in Rheumatic fever.
What is Parkinson's disease?
Parkinson's disease is a degeneration of the substantia nigra, which is an area of the midbrain that transmits dopominergic projections to the striatum(caudate, putamen).
The actual loss of dopamine input to the striatum often results in what symptomatic pjhysical triad seen in Parkinson's disease?
The symptomatic triad of :
Bradykinesia-slow movement
Resting tremor
Cogwheel rigidity.
other physical symptoms and signs associated with PD, are hunched over gait, with difficulty starting and stopping and even turning while actively walking.
Dopominergic projections to the striatum synapse on two pathways. What are they?
The two pathways are the Direct and indirect pathway.
What is the direct pathway?
The direct pathway is an internal segment on the globus pallidus(GPi)- ventrolateral nucleus of the thalamus(VL)- motor areas of the cerebral cortex.
What is the indirect pathway regarding dopominergic projections?
The indirect pathway involves an external segment of the globus pallidus(GPe), a subthalamic nucleus(STN)-GPi-VL-motor areas of the cerebral cortex.
The direct pathway excites the cortex and the indirect pathway inhibits it.
TRUE. The result of normal dopominergic input to the striatum is increased cortical excitation.
Logically, loss of dopamine from substantia nigra degeneration in PD will lead to what?
Loss of dopomine will lead to decreased activity of the direct pathway and increased activity of the indirect pathway.
In Parkinson's disease, there is decreased excitation of the cortex and increased inhibition of the cortex. TRUE/FALSE
TRUE. The result is an overall decrease in motor cortical activity that results in bradykinesia and rigidity.
PD disinhibits the indirect pathway, allowing it to inhibit the cortex.
Overall, one can say that PD involves a shortage of what?
PD involves a shortage of dopomine. Treatment involves the restoration of dopomine either directly(L-dopa) or indirectly.
If indirect strategies include agonists of the dopomine receptors, what are some drugs used as agonists of the dopomine receptors?
Med Tx: Paralytic Ileus
What is a typical disease that may result from too much dopomine?
Schizophrenia is occasionally caused by too much dopomine. Hallucinations may result.
If too much dopomine can lead to hallucinations, the corollary is that dopomine antagonists used in the treatment of schizophrenia may lead to what?
Dopomine antagonists may lead to dyskinesias(abnormal movements).
Why are dopomine agonists used occasionally to treat prolactinomas?
Dopomine often inhibits prolactin.
Why are dopomine agonists used occasionally to treat prolactinomas?
Dopomine often inhibits prolactin.
What may be a cause of an isolated seizure?
Isolated seizures may arise from abnormal electrical impulses in the brain. Additional causes may be the result of electrolyte or glucose, medications, drug withdrawal, head trauma, infections, fever, stroke and space occupying lesions such as tumors.
Disorders of decreased inhibition/increased excitation in the brain can result in epilepsy or recurrent staging seizures. TRUE/FALSE
TRUE. Ion channel disorders such as channelopathies may be responsible as well.
What is meant by the term "idiopathic seizure"?
Idiopathic usually means that no specific cause can be identified. Though there is always a reason for a seizure, the exact cause is not always known.
Is a seizure and syncope the same thing?
Seizures and syncopes are two distinct occurrences.
Syncope is fainting, which in itself may be caused by a variety of factors.
The presence of an aura(but not always)(visual, olfactory or auditory, tongue biting, loss of bladder or bowel control and uncoordinated motions may all be typical of a seizure pattern.
Do single isolated seizures always require treatment?
No. However, an underlying cause should be sought.
What do antiepileptics do?
Antiepileptics either inhibit excitation of neurons or increase inhibition of them.
What is the main excitatory neurotransmitter in the brain?
Glutamate is the main excitatory neurotransmitter in the brain.
GABA is the main inhibitory one.
How might glutamate be inhibited?
Glutamate may be inhibited by decreasing its release from the presynaptic neuron from responding.
How might one inhibit the release of glutamate?
It is possible to inhibit calciuym channels of the presynaptic neuron that permit the Ca+ influx that leads to synaptic vesicle fusion/release of neurotransmitter. Ethosuximide is one example.
Can sodium channels be inhibited for the purpose of inhibiting glutamate?
Yes.Sodium channels stimulate the action potential in the presynaptic neuron. Drug examples are Phenytoin, Carbamezapine and Valproic acid.
Topiramate will block post-synaptic neurons which blocks the AMPA glutamate receptor.
What can be done to increase GABA or its effectiveness?
To increase GABA, it is possible to decrease synaptic degradation of GABA(vigabatrin) or block GABA reuptake in the presynaptic neuron(tigabine).
Benzodiazopines and barbiturates act at which specific chloride channel?
These act at the post-synaptic chloride channel where GABA acts. They accentuate chloride influx, thus increasing inhibition, and decreasing the firing of these neurons.
Why can almost anytype of cranial bleeding increase intracranial pressure?
The intracranial space is limited, so lesion occupying structures such as tumors, edema from infection, stroke and inflammation may all be responsible for elevating intracranial pressure,
Cite some signs and symptoms of ICP.
Visual changes, nausea, headache, seizures, behavioral changes and neurological deficits.
What is Papilledema?
It is the swelling of the optic nerve as a result of ICP elevation.
Is brain herniation possible with very high ICP?
Yes. Very high ICP can cause brain herniation through the foramen magnum. This can result in the rapid onset of certain neurological symptoms and signs such as, fixed or dilated pupil, hemiparesis, coma or death.
What is a common treatment for elevated ICP?
I/V mannitol is often employed. mannitol increases the osmolarity of the blood so as to draw water from the edema into the blood.
Can lumbar punctures be routinely employed for increased ICP?
Lumbar punctures can be risky. Lumbar punctures can create negative pressure, in the spinal canal that may encourage herniation.
Why do many patients undergo a CT scan before undergoing lumbar puncture?
CT scans are recommended to search for signs of ICP elevation. such as caused by ventricular dilatation.
Where is CSF produced?
CSF is produced by the choroid plexus. It circulates through the ventricles and basically bathes the brain.
CSF production is in equilibrium with its reabsorption back into the venous system via the arachnoid granulations. Is this a true statement.
This is true. A disturbance in the CSF equilibrium may cause hydrocephalus and may elevate ICP.
What are some causes of hydrocephalus?
Hydrocephalus may be caused by increased CSF production, choroid plexus tumor, decreased CSF reabsorption(blockage of arachnoid villi), from subarachnoid hemorrhage or infection or ventricular obstruction.Ventricular tumors of congenital formation are referred to as Arnold-Chiari, or Dandy-Walker syndrome.
Obstructive causes of hydrocephalus, as from tumors are referred to as non-communicating forms of hydrocephalus. TRUE/FALSE
TRUE. Obstructive causes of hydrocephalus, as from tumors are referred to as non-communicating forms of hydrocephalus.
What are some signs and symptoms of hydrocephalus?
Visual disturbances, papilledema, headache, urinary incontinence, unsteady gait, mental status changes, hypertension, bradycardia and/or irregular respiration.
What is the Cushing's triad?
Cushing's triad consists of hypertension, bradycardia and irregular respiration. Due to the compressed areas, these symptoms are more easily activated.
What is the treatment for hydrocephalus?
Treatment requires removal of CSF via lumbar punture(in communicating hydrocephalus), or the placement of a shunt from the ventricular system that drains either into the abdomen or the atrium of the heart(in obstructive hydrocephalus).
Pseudotumor cerebri (PC) is also known as Idiopathic benign intracranial hypertension. TRUE/FALSE
TRUE. Pseudotumor cerebri is also known as Idiopathic benign intracranial hypertension.
In Pseudotumor cerebri symptoms and signs of elevated ICP are present but the brain appears normal when scanned. TRUE/FALSE
TRUE. There is no ventricular enlargement as in hydrocephalus.
Where is PC most commonly seen?
PC is most commonly seen in women, especially obese women.
What are some symptoms of PC?
headaches and visual changes are typical, nausea, vomiting, papilledema and elevated ICP on lumbar puncture.
What is a common mode of therapy for PC?
Acetazolamide, a carbonic anhydrase inhibitor, is often used for treatment. This is thought to decrease CSF production, leading to a decrease in ICP.
In the skull, what does the dura mater adhere tightly to?
The dura mater adheres tightly to the inner surface of the skull, but there is some space between it and the posterior aspect of the vertebrae in the spine.
The subdural space lies between the dura mater and the arachnoid. TRUE/FALSE
TRUE. The subarachnoid space is the space between the arachnoid and the pia mater, which adheres directly to the brain.
Which space contains the CSF?
The subarachnoid space contains CSF. Any infection or hemorrhaging can occur in any of these places or in the barin itself.
How may infectious agents arrive at the brain? What regins are most responsible for this spread?
Infectious agents may arrive via hematogenous spread. The meninges may be infected as well. Endocarditis, pneumonia, sinusitis, orbital cellulitis or severe cases of otitis, osteomyelitis,paraspinous abscess, or psoas abscess, or from trauma or surgery.
Irritation of the meninges, as in subarachnoid hemorrhage or meningitis can lead to pain during any maneuver that puts traction on them. TRUE/FALSE
TRUE. Meningeal irritation may cause a stiff neck.
What is Brudzinski's sign?
On physical exam, if one attempts to flex the patients neck, this may result in involuntary flexing of the hip and knees. This is Brudzinski's sign.
What is Kernig's sign?
If the thigh is flexed at the hip, and ten attempts to straighten the patients leg at the knee, this is met with resistance. This is Kernig's sign.
What is amajor cause of epidural hematomas?
Epidural hematomas are caused by trauma? usually the middle meningeal aretery is ruptured. This causes bleeding between the skull and the dura mater.
What are some symptoms of epidural hematoma?
headaches, nausea and vomiting are common symptoms. Seizures are possible as is an increase in intracranial pressure.
What is the lucid interval considered?
Occasionally patients with epidural hematomas maintain or regain consciousness for a period of time post trauma. Relapsing unconsciousness and coma may follow lucid intervals.
What is the treatment for epidural hematoma?
Blood is drained surgically by drilling burr holes in the skull. Pooled blood will place abnormal pressures on the cerebrum resulting in coma and death if immediate treatment is not sought.
How are epidural abscesses spread?
Epidural abscesses are caused by hematogenous spread from nearby infection.
What type of infections might result in epidural abscesses?
Osteomyelitis, paraspinous abscess, or the psoas muscle in the spine, sinusitis, orbital cellulitis, or otitis in the skull. Neurosurgical procedures might result in epidural abscesses, though rarely.
What are some symptons of EAs?
Elevated ICP, headache nausea and vomiting, focal neurological signs and seizures.
What type of symptoms might be noted in spinal epidural abscesses?
back pain, radicular pain(pain radiating along a dermatomal distribution, and bowel/bladder incontinence is possible as well.
Why are spinal epidural abscesses more likely to occur than intracranial abscesses?
There is more space between the dura mater and overlying bone in the spine than in the cranium,(where the dura is tightly adherent to the skull).
What are common pathogens in epidural abscesses?
Staph. aureus and Streptococcus are quite common in epidural abscesses. Surgical drainage and antibiotics are common modes of treatment.
طاوِلَة - ات
What are some predisposing conditions of subdural hematomas?
Thrombocytopenia, clotting disorders and alcoholism(trauma from a fall) may predispose to a subdural hematoma.
Symptoms such as intracranial pressure and focal neurological defects are typical of subdural hematoma. TRUE/FALSE
TRUE. Symptomsmay be acute or chronic, over weeks or months.
What is a more common cause of subdural hematoma in the elderly?
Subdural hematoma may be caused by brain atrophy, which extends abnormally the bridging veins, predisposing them to spontaneous rupture.
Surgical drainage of subdural hematomas are a common therapeutic protocol. TRUE/FALSE
What causes subdural abscesses?
Subdural abscesses can arise by the spread of infectious material from intracerebral abscesses, meningitis, sinusitis, trauma surgery, intracerebral infections, otitis or hematogenous spread from a distant site.
What are the most commonly seen bacterial organisms in subdural abscesses?
Staph. aureus, Strreptococcus and gram negative bacteria.
Antibiotics and possible surgical drainage may be required.
When are subarachnoid hemorrhages seen?
Subarachnoid hemorrhages are seen secondary to rupture of an aneurysm or less frequently to a rupture of an arteriovenous malformation(AVM).
Suddeen onset of a severe debilitating headache is a common complaint with subarachnoid hemorrhage. TRUE/FALSE
How is diagnosis acheived in subarachnoid hemorrhage?
Blood seen in the CSF, on lumbar puncture and evidence of bleeding on CT or MRI scans.
What is the therapeutic approach to subdural hemorrhages?
Patients are stabilized and prepped for surgical clipping of the aneurysm or intravascular coiling. Intravascular coiling is a procedure that blocks off the aneurysm with microcoils.
What is meningitis?
Meningitis is an infection of the meninges and CSF from hematogenous spread; Strep. pneumoniae from pneumonia,N. meningitidis or ear infection, H. influenzae, or post surgery or trauma such as Staph. or gram negatives.
What are the most common organisms responsible for meningitis?
In neonates: group B strep.
In children: H. influenzae, Strep pneumoniae, N. meningitidis.
In adults: Strep. pneumoniae, N. meningitidis.
Tbc and Listeria may cause meningitis as well.
When does viral meningitis become an issue?
Viral meningitis such as enterovirus, varicella zoster virus, herpes simplex, HIV and fungal meningitis such as cryptococcus, candida, histoplasmosis are more commonly seen in immunocompromised patients. Non bacterial causes are more subacute in nature.
What is Intraparynchymal hemorrhage?
Intraparenchymal hemorrhage may be caused by hypertension, trauma, aneurysm/arteriovenous malformation rupture, intracranial tumor bleeding and post stroke bleeding.
When might a brain abscess arise?
A brain or cerebral abscess may arise when infections spread to the brain from nearby infections(meningitis, sinusitis, otitis or during surgery.
What are some symptoms of brain abscesses?
Fever, headache, nausea and vomiting with possible seizures and neurological deficits and mental status.
What organisms may cause cerebral abscesses?
Staph. aureus, Streptococcus, anerobes, H. influenza, tbc, fungi and certain protozoans may cause cerebral abscesses.
What is the usual cause of encephalitis?
The cause of encephalitis is usually viral(herpes simplex, enterovirus, mumps, rabies, West Nile virus and St. Louis encephalitis.
Can other organisms cause encephalitis?
Certain parasites such as toxoplasmosis, and some forms of bacteria, Listeria, Bartonella, Rickettsia and Mycoplasma.
Encephalitis often shares the same symptoms as seen in other brain insults and infections. TRUE/FALSE
How is diagnosis often acheived for encephalitis?
Evidence of the infectious agent in the CSF or via brain biopsy.
How is treatment approached for encephalitis?
Treatment is aimed at the particular offending agent, such as acyclovir for herpes simplex virus, if possible. Symptomatic treatment is also employed when necessary.
What is a key procedure in the diagnosis of suspected meningitis/encephalitis?
Examination of CSF via lumbar puncture.
What standard CSF parameters are usually abnormal in almost any form of meningitis?
WBC count and protein levels will be elevated in meningitis.
What type of cellular change is often seen in bacterial meningitis?
In bacterial meningitis there is usually a predominanace of PMNs(polymorphonuclear cells).
In a fungal or viral meningitis there is an elevation in mononuclear cells.
Gram stain is employed to identify bacterial pathogens and PCR(polymerase chain reaction) is used to identify viral agents. TRUE/FALSE
TRUE. Gram stain is employed to identify bacterial pathogens and PCR(polymerase chain reaction) is used to identify viral agents.
Tbc and bacteria may cause a decrease in CSF glucose to less than 2/3 the amount of serum glucose. Is this statement accurate.
This statement is true.Tbc and bacteria may cause a decrease in CSF glucose to less than 2/3 the amount of serum glucose.
Blood in the CSF can idicate what condition?
It may indicate intracranial bleeding, such as subarachnoid hemorrhage.
How might one differentiate blood in CSF as caused by intracranial hemorrhage or from the CSF tap?
In a lumbar puncture, multiple tubes of CSF are take. If the tap is traumatic, the quantity of blood in the CSF samples will decrease with each successive tube. If intracranial bleeding is present, the amount of blood in each tube will be constant.
Blood that is present in the CSF for more than 6 hours, is usually broken down, giving the CSF a yellowish color(xanthochromia). TRUE/FALSE
TRUE. Blood arising from trauma of the tap will not have had time to break down, and xanthochromia will not be present.
Define "meningioma".
These are benign tumors that can occur on any portion of the meninges resulting in any neurological symptom.
How are meningiomas treated?
Meningiomas are treated with surgery or radiation.
What is an acoustic neuroma?
These are also known as vestibular schwannomas. These are benign tumors of cranial nerve V111(vestibulocochlear).
What are some symptoms of acoustic neuromas?
They may cause unilateral hearing loss, vertigo, and/or other cranial nerve deficits if the tumor is compressing the brainstem.
What is meant by the term "Gliomas"?
Gliomas include: astrocytoma(including glioblastoma multiforme, oligodendroglioma and ependymoma.
Where do ependymomas originate from?
Ependymomas originate from cells of ventricular lining and may result in obstruction/hydrocephalus.
Can CNS lymphomas be of primary origen?
Yes. CNS lymphoma occurs most commonly in immunocompromised patients(AIDS or from secondary metastasis from another lymphomatous site.
Gliomas occur commonly in the cerebral hemispheres. TRUE/FALSE
TRUE. They can occasionally occur elsewhere in the brain.
What is a medulloblastoma?
These are childhood tumors that in contrast, occur most commonly in the cerebellum.
Blockage or occlusion of cerebral vasculature from plaque formation, emboli or thrombosis may result in acute cerebral ischemia(stroke). TRUE/FALSE
TRUE. Blockage or occlusion of cerebral vasculature from plaque formation, emboli or thrombosis may result in acute cerebral ischemia(stroke).
List 5 possible causes of cerebral ischemia.
1. Emboli
2. Atherosclerotic plaque
3. Venous occlusion
4. Arterial dissection
5. Severe hypotension
How might atherosclerotic plaque result in stroke?
Atherosclerotic plaque can occlude the carotid arteries or the vertebro-basilar system or their branches.
What are watershed infarcts?
Severe hypotension, which may be caused by cardiac dysfunction. This may lead to infarction of cerebral areas at the boundaries of the major vascular territories(watershed infarcts).
What is a transient ischemic attack?(TIA)
These may be a warning of a more serious stroke to come.Narrowing of the carotid or vertebrobasilar system or small pieces mof plaque that embolize can cause stroke like symptoms, that last for several seconds, minutes or hours.
Define "Amaurosis fugax".
Amaurosis fugax is a typical TIA symptom. Transient ischemia in the opthalmic artery(branch of the internal carotid) causes temporary blindness. retinal attachment may be described in a similar way.
What might be a logical therapeutic approach to TIAs or minor strokes?
Therapy for the acute form with thrombolytics and prevention of future events. Lowering of blood pressure, quitting smoking , decreasing cholesterol via a low fat diet, and taking aspirin to inhibit platelet aggregation.
The common carotid arteries branch to form which subsequent arteries?
The external and internal carotid arteries.
The internal carotids give rise to which arteries?
Middle and anterior cerebral arteries.
The middle cerebral arteries supply what part of the cerebral hemisphere?
They suppl;y much of the lateral surfaces of the hemispheres. The anterior cerebrals supply much of the medial surfaces.
Regarding posterior circulation, the vertebral arteries arise from these arteries. What are they?
The subclavian arteries.
What do the vertebral arteries feed?
They feed the medial medulla and give off the posterior inferior cerebellar arteries(PICAs). This last arterial tree supplies the lateral brainstem and inferior cerebellum.
How is the basilar artery formed?
The vertebral arteries fuse over the medulla to form the basilar artery.
What does the basilar artery feed?
It feeds the medial pons and gives off the AICAs(anterior inferior cerebellar arteries, which feed the lateral portions of the pons and the anterior cerebellum.
Which artery gives rise to the superior cerebellar arteries?
The basilar artery gives rise to the superior cerebellar arteries. These supply the brainstem and cerebellum, before splitting into the posterior cerebellar arteries, which supply the occipital bones.
The posterior communicating arteries link the anterior and posterior circulation circulation, creating what important structure?
The circle of Willis.
A stroke of the middle cerebral artery will affect which regions of the body?
The face, the arm, and to a lesser extent, the leg. All are on the contralateral side because we are far above the decussation in the medulla.
A stroke of the anterior cerebral artery will result in what?
An anterior cerebral arterial stroke will result in sensory and motor dysfunction that is greater in the leg than in the arm(contralateral side).
define "abulia'.
Abulia is a lack of motivation due to ischemia/infarction of a part of the frontal lobe. Anterior cerebral arterial strokes may cause abulia.
What important speech related structures does the left hemisphere house?
This area is responsible for language production(Broca's area) and comprehension(Wernicke's area).
Where do Broca's and Wernicke's area receive their blood supply from respectively?
Broca's supply is from the antyerior branch of the middle cerebral artery, and Wernicke's comes from the posterior branch of the middle cerebral artery.
What is Broca's aphasia?
In this condition, there is difficulty producing spoken and written language, but comprehension is preserved.
What is Wernicke's aphasia?
This is considered a receptive aphasia. There is difficulty understanding language(both written and spoken). Speech appears to occur normally, but there is a senselessness to the speech pattern. There is as well an inability to follow commands.
What is Dysarthria?
Certain lesions at a variety of locations and arterial structures may result in this. Dysarthria is a problem producing mouth and tongue movements necessary for speech. The spoken and written language are still understood.
What are lacunar infarcts/
Lacunar infarcts involve the small penetrating branches that nourish deeper brain structures.
These strokes may result in isolated motor or isolated sensory deficits.
What is a rather simplified way of defining Multiple Sclerosis(MS)?
The myelin of nerves is likened to wire insulation. In MS, the insulation is damaged, and nerve transmission is greatly debilitated.
How might one describe the pathophysiology of MS?
There is no clear pathophysiologic explanation. It has been assumed that autoimmunity and/or genetics might be a factor of cause.
How does one justify the term "multiple" in MS?
Multiple refers to to the characteristic multiple lesions in multiple sites in the CNS.
What is the most common clinical course of the disease?
It is the relapsing-remitting course, which develops in a series of normal periods accentuated by flares.
The loss of myelin leads to a slowing of nerve conduction. TRUE/FALSE
TRUE. The loss of myelin leads to a slowing of nerve conduction.
Can symptoms of MS be generally defined?
Not really. Symptoms will vary depending on the site of the lesion. Subcortical white matter lesions can result in cognitive dysfunction.
Brainstem lesions result in cranial nerve dysfunction. Certebellar lesions result in ataxia, dysdiadochokinesia.
MS spinal tract lesions will result in what kind of symptoms?
Pain, temperature and vibration sense loss and or motor dysfunction.
MS is limited to the CNS. The PNS is rarely affected. Is this statement accurate?
Yes. MS is limited to the CNS. The PNS is rarely affected.
Are LMN affected in MS?
No. UMN are affected in MS which can cause spasticity, increased reflexes, Babinski's sign etc.
The bladder has UMN(in the spinal cord) and LMN arising from sacral levels 2-4(S 2,3,4) which travel in peripheral nerves. TRUE/FALSE
TRUE. UMN lesions of the bladder cause spaticity of the bladder, which may present as urinary frequency and urgency.
What is Uthoff's phenomenon?
In MS, this is a worsening of symptoms in the heat(weakness or sensory changes after a hot bath or vigourous exercise.
What is L'Hermitte's sign?
This is when electrical sensations run down the spine when the patient bends the head forward.
MS is also a common underlying cause of internuclear ophthalmoplegia(INO). TRUE/FALSE
TRUE. MS is also a common underlying cause of internuclear ophthalmoplegia(INO).
Where might the demyelinating lesion be in INO associated with MS?
For INO, the lesion must be in the MLF ipsilateral to the eye that cannot adduct when the other eye abducts(though it still adducts on convergence.
What is the general therapeutic approach for MS?
Treatment is immunomodulatory. Intrferon and/or glatiramer acetate(Capaxone).
What is Glatiramer acetate?
Glatiramer acetate is a mixture of small peptides related to proteins in myelin. Its mechanism of action is believed to occur by modifying the immune processes involved in the pathogenesis of MS.
The spinal cord's white and gray matter is reversed as compared with the brain. TRUE/FALSE
TRUE. In the spinal cord, the white matter runs on the outside and the gray matter is in the inside.
What is meant by spinal lamination?
Within the tracts of the spinal cord, the fibers from different regions of the body are aligned in a specific way. This is lamination.
What is meany by generalized radiculopathy?
Discs that prolapse and impinge on either a sensory or motor root can cause isolated sensory or motor symptoms in a dermatomal distribution.
How might nerve roots become depressed?
Nerves roots may become depressed by herniation, prolapsing, tumors or spinal stenosis.
A prolapsed disc usually affects which adjacent disc?
A prolapsed disc usually affects the root below it, so the L4 disc hits the L5 root, and the L5 will affect the S1.
In nerve root compression, sensory findings tend to occur where?
In nerve root compression, sensory findings occur only in the dermatome of the affected root.
In nerve root compression, sensory findings tend to occur where?
In nerve root compression, sensory findings occur only in the dermatome of the affected root.
What are some commonly tested reflexes?
Triceps is controlled by C7/8.
Biceps and brachioradialis are controlled by C5/6.
Patellar reflex and knee extension are controlled by L3/4.
S1/2 initiate ankle reflex and plantar flextion.
The axons of anterior horn cells(LMNs) exit the spinal cord anteriorly(ventrally) as the anterior or ventral roots. TRUE/FALSE
True. The axons of anterior horn cells(LMNs) exit the spinal cord anteriorly(ventrally) as the anterior or ventral roots.
The peripheral nerves generally carry both motor fibers traveling to the muscles and sensory fibers from the skin, joints and muscles.
Sensory fibers carry or transmit generally what type of information?
They return information about, light, touch, pain temperature and proprioception.
Motor neuron axons traveling in peripheral nerves eventually synapse where?
These nerves eventually synapse with muscle cells at the neuro-muscular junction. Only excitation is possible at the NMJ and the neurotransmitter is acetylcholine.
If muscular weakness involves damage to LMNs(anterior horn cells, nerve root or peripheral nerves, what might one expect symptomatically?
One should expect LMN signs, such as fasciculations, decreased absent reflexes and muscle atrophy.
Peripheral neuropathy typically leads to what type of regional muscular weakness?
Peripheral neuropathy typically leads to distal muscle weakness. Myopathies usually lead to proximal muscle weakness.
Weakness and sensory changes together can only occur with what type of lesions?
This condition might be the result of lesions of peripheral nerves, the cerebral hemispheres, middle cerebral aretery stroke, or brainstem or a spinal cord lesion that affects both motor and sensory pathways(Transverse myelitis in MS).
How might the following be explained? Should there be a loss of motor function and light touch/proprioception on one side and pain/temperature sensation loss on the opposite side, what type of lesion might this be?
This would indicate a spinal cord lesion.
Weakness alone without sensory changes might imply a problem specifically affecting which pathways?
Weakness alone without sensory changes might imply a problem specifically affecting motor pathways(pure motor stroke, ALS(amyotrophic lateral sclerosis), the NMJ or the actual muscles themselves.
The juvenile spinal muscular atrophy syndromes affect the anterior horn cells. TRUE/FALSE
TRUE. The juvenile spinal muscular atrophy syndromes affect the anterior horn cells. Weakness, flaccid paralysis, fasciculations, muscle atrophy with decreased or absent reflexes are seen. Poliomyelitis might also affect anterior horn cells.
Does ALS(amyotrophic lateral sclerosis) also affect horn cells?
Yes. It also affects anterior horn cells as well as the corticospinal tract.
Considering what is affected in ALS, what kind of neuronal findings might one expect to find?
Both upper and lower motor neuron findings. Weakness, spastic paralysis, some increased reflexes, and some decreased.
Peripheral neuropathy may be caused by damage to what specific neuron tissue?
Peripheral neuropathy can be caused by damage to either to the axons themselves or the myelin(Guillain-Barre is an example of a demyelinating peripheral neuropathy.
What type of studies might help distinguish between axonal and demyelinating causes of neuropathy?
Nerve conduction studies might help distinguish between axonal and demyelinating causes of neuropathy.
Regarding axonal and demyelinating causes of neuropathy, one process slows nerve conduction, while the other decreases the amplitude of nerve conduction. If this is true, explain why.
This statement is true. Myelin insulates the axon so as to allow for faster nerve conduction. So myelin loss decreases the velocity. Axonal damage will decrease the amplitude of nerve conduction.
What is meant by a "mononeuropathy"?
A mononeuropathy is a problem limited to one nerve. This might indicate entrapment, such as the median nerve in carpal tunnel.
What is mononeuropathy multiplex?
Mononeuropathy multiplex involves multiple individual mononeuropathies such as seen in a systemic underlying pathology such as diabetes, vasculitis, infection or toxicity(lead).
Peripheral neuropathy(multiple distal portions of nerves affected, such as "stocking glove" distribution may also result from a systemic pathology such as diabetes or a systemic toxic reaction. TRUE/FALSE
TRUE, Peripheral neuropathy(multiple distal portions of nerves affected, such as "stocking glove" distribution may also result from a systemic pathology such as diabetes or a systemic toxic reaction.
What is Myasthenia gravis?
In MG autoantibodies are produced against the acetylcholine receptors on muscle cells at the neuromuscular junction(NMJ).
Why do the antibodies create a problem for muscular function?
The antibodies block the receptor so that acetylcholine cannot bind and stimulate muscular contraction.
What is a possible cause of MG?
Most cases of MG are idiopathic. Occasionally MG may be observed secondary to thymus tumors such as Thymoma.
What are some observable signs and symptoms of MG?
MG can cause general weakness. Muscles are likely to more easily fatigue. Facial muscles are affected which can result in ptosis(drooping eyelids) with quick eyelid fatigue during extended upward gazes(ptosis time), with trouble swallowing and dysarthria(speaking difficulty).
Even extended arm abduction may be difficult for the patient.
In MG, one doesn't generally see sensory deficits as might be present in peripheral neuropathy. TRUE/FALSE
TRUE. As well, pain may be present in inflammatory muscle disease.
How is MG diagnosed?
MG is confirmed by detecting the acetylcholine receptor antibody in the blood or by EMG(electromyelography) study which demonstrates fatigue during repetitive stimulation.
What is Tensilon?
tensilon, also called edrophonium, is a competitive inhibitor for binding sites on acetylcholinesterase, which increases the life of acetylcholine in the synapse. It acts rather quickly.
Is the Tensilon absolute proof of MG?
No, but it is still considered a very reliable indicator. Almost anyone with muscle weakness might feel a little better from increased stimulation of their muscles by acetylcholine.
What is pyridostigmine?
Pyridostigmine is one treatment for MG.It blocks acetylcholinesterase. It will have no effect on the underlying cause, which is the immune syste.
Occasionally, immunosuppression is employed if the condition is severe. Removal of the thymus is might improve the condition.
What is Lambert-Eaton syndrome? (LES)
LES may occur secondary to certain malignancies.(Paraneoplastic syndromes).
LES is commonly seen with what type of cancer.
LES is often seen with small cell lung cancers. It may be seen with other forms as well.
What is the pathophysiology of LES?
It is somewhat different from MG. In LES autoantibodies form against the presymaptic calcium channels, leading to decreased synaptic activity at the NMJ.
Are the symptoms of LES similar to LES?
As in MG, there is weakness, though the muscles og the face are not as severely affected.
In LES, because the problem of failure is due to Ca+ influx to trigger acetylcholine release, repetitive stimulation actually produces transient improvement. TRUE/FALSE
TRUE. This is the opposite of what happens in MG.
Unless it is caused by injury, muscle problems tend to be fairly symmetrical. TRUE/FALSE
TRUE. Muscle problems also tend to present with proximal weakness, as opposed to distal weakness often seen in neuropathies.
What are the three major categories of muscle disease?
The three major categories of muscle disease are:
2.Inflammatory myopathies
3.Metabolic myopathies.
What are the dystrophic muscle diseases?
These diseases are usually genetic by nature with specific patterns of affected areas. Duchenne's muscular dystrophy, myotonic dystrophy and fascioscapulohumeral dystrophy.
What are inflammatory muscular diseases?
These include dermatomyositis and polymyositis.
What are metabolic myopathies?
These include mitochondrial myopathies and glycogen storage disease syndromes.
Steroid induced as well as endocrine induced myopathies are included here. Endocrine myopathies as caused by hyper or hypothyroidism.
Inflammatory muscle diseases typically cause muscle pain and tenderness. TRUE/FALSE
TRUE. Muscle pain and tenderness might help to differentiate or distinguish myopathy from neuropathy or myasthenia as the cause of weakness.