Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuroendocrine > NE Exam 2 Clinical > Flashcards

NE Exam 2 Clinical Flashcards

1
Q

SC lesions to Fascicule Gracile & Cuneatus?

Sensory Ataxia?

A

SC lesions result in ipsilateral reduction or loss of discriminative, positional, & vibratory tactile sensations at & below the segmental level of injury

Sensory ataxia, loss of muscle stretch (tendon) reflexes, & proprioceptive losses from the extremities due to lack of sensory input. Patient may also have a wide-based stance & may place the feet to the floor with force, in an effort to create the missing proprioceptive input

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Blood supply to the Primary Somatosensory Cortex is provided by the anterior & middle cerebral arteries

MCA & ACA lesions cause?

A

MCA lesions produce tactile loss over the contralateral upper body & face

ACA lesions cause loss of sensation to the contralateral lower extremity.

Due to the somatosensory homunculus, lesions to arteries then different deficits:
Middle cerebral artery - lateral, face, mouth throat
Anterior cerebral artery - more medial, foot, LE, hip
Remember we are on opposite side of the body!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Agnosia

A

Parietal cortical regions also receive tactile inputs:
•Lesions in parietal association area can produce agnosia
•Contralateral body region(s) lost from body map
•Limb is not recognized as part of the patient’s own body
•Sensation is not radically altered

Stroke is a vascular effect.
Don’t recognize own body. Don’t know what the limb is doing, less movement because you forgot the limb exists.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Alzheimer’s Disease

A

Most common neurodegenerative disease,
incidence increases with age
•Typical presentation is 70+ years

Symptoms:
•Memory failure, progressing steadily to involve motor skills, speech &
sensation
•Etiology is unknown, small proportion of
cases have a genetic association
•Striking thinning of gyri, particularly those
of the frontal and temporal lobes

Plaques, neurofibrillary tangles & neuronal loss are
identified on sections:
•Amyloid (amyloid β) plaques: amorphous , pink
masses in the cortex
•Neurofibrillary tangles : flame shaped skeins formed
by abnormal accumulation of tau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Parkinson’s Disease

A

Parkinson’s: loss of neuro melanin pigment so have difficulty producing enough dopamine from these cells, which decreases the amount of dopamine released to other areas of the brain to regulate movement

So you have movement disorder, can worsen overtime

Lewy body impairs function of cell and overtime leads to loss of neuromelanin pigment

Clinical features: tremor, slow movement, & rigidity resulting from degeneration of neurons in the substantia nigra → loss of dopamine (etiology unknown)

Distinctive inclusions are seen in the remaining neurons, Lewy bodies
•Rounded , pink staining inclusions, w/ pale halo
•Composed of aggregates of the protein alpha synuclein & other proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Holoprosencephaly (HPE)

A

Holoprosencephaly (HPE) is a cephalic disorder in which the prosencephalon (the forebrain of the embryo) fails to develop into two hemispheres.

Incomplete separation of the cerebral hemispheres & most cases are associated with
facial abnormalities

•Cyclopia, premaxillary agenesis, proboscis,
single nostril, hypotelorism, facial clefts

•Severe & relatively common defect, 1:250 fetuses & 1:15,000 neonates

•Over 12+ genetic loci have been implicated:
SHH, GLI, IHH, SIX3, TGIF, ZIC, PTCH. However, SHH is the main player in this

•Impaired forebrain development, → impacts
FNP development → facial anomalies

__________________
HPE:

Prosencephalon (single structure) –> splits into telencephalon and diencephalon –> telencephalon splits into right and left hemispheres

when Telencephalon has problems in splitting into right and left hemispheres. Called HPE

Varying levels of severity bc numerous genes involved

HPE in the most severe case, would lead to fetal death. In least severe, some mental decline or a single front tooth.

Caused by loss of SHH

SHH is the key player in this
The other genes either positively or negatively impact sonic

HPE is one of the most common conditions of malformation of the face, but not reported as much bc many of the fetuses die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Agenesis of Corpus Callosum

A

Complete or partial absence of the
corpus callosum

•The condition may be asymptomatic, but
seizures & mental deficiency are common.

•Associated with more than 50 human congenital syndromes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Lissencephaly

A

not very common

  • Incomplete neuronal migration during 3 4 months of gestation
  • Incidence of 1:100,000 live births
  • Infant will initially appear ‘normal’ but later develop seizures, profound mental deficiency, & mild spastic quadriplegia

Leads to severe developmental disabilities and even seizures and paralysis at times

“Smooth” cerebral surface exhibiting:
• Pachygyria, broad, thick gyri
• Agyria, lack of gyri
• Neuronal heterotopia: cells in aberrant positions
compared to a normal brain
• Enlarged ventricles & malformation of the corpus
callosum are common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Microencephaly

A
  • Neurodevelopmental disorder where calvaria & brain are small, but face is normal sized
  • Results from a reduction in brain growth. Lack of coordinated brain and skull growth
  • Inadequate pressure from the growing brain leads to a small neurocranium
  • 1: 25,000 infants/year in the US
  • Accompanying mental deficiencies

Causes:
• Autosomal recessive primary microcephaly
• Ionizing radiation
• Infectious agents (cytomegalovirus , Zika virus,
rubella virus, Toxoplasma gondii
• Maternal alcohol abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Damage to prefrontal association areas in brain

A

Damage to this area can result in drastic personality changes

Prefrontal association areas are concerned with emotion, motivation, personality, initiative, judgement, ability to concentrate, and social inhibitions

Cingulate gyrus also modulates emotional aspects of behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Damage to Cerebellum

A

Results in problems with equilibrium, postural control, and equilibrium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lesions of the Trigeminal Nerve/Nuclei

A

CLINICAL: Lesions of the Trigeminal Nerve/Nuclei

Unilateral lesion :

1) Anesthesia and loss of general sensations in the trigeminal dermatomes
2) Paralysis of the muscles of mastication
3) Loss of ipsilateral afferent limb of corneal reflex

Alternating trigeminal hemiplegia:

1) Unilateral destruction of the trigeminal nerve & CST in the pons
2) Ipsilateral trigeminal anesthesia & paralysis, & contralateral spastic hemiplegia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lateral Medullary Syndrome** (a.k.a. PICA syndrome or Wallenburg Syndrome)

A

Lateral Medullary Syndrome** (a.k.a. PICA syndrome or Wallenburg Syndrome)

Deficits: Contralateral loss of pain & thermal sensation (body)

Vascular Territory:

  • -Occlusion of PICA and/or its branches
  • -Occlusion of vertebral artery at the origin of the PICA, blocking PICA flow

CL loss of pain and temperature to BODY (ALS)

IL loss of pain and temperature to FACE and oral cavity (spinal V tract/nucleus)

IL Horner’s (hypothalamospinal fibers)

Loss of Nucleus Ambiguus (CN 9 and CN 10) –> loss of gag reflex, hoarseness, uvula deviated CL

Nausea, diplopia, tendensity to fall on IL side, nystagmus, vertigo (vestibular nuclei)

IL unsteadiness (ataxia) –> loss of restiform body

_______________________
Dissociated sensory loss: loss of one sensory modality but another is within normal limits

Deficits:
• Contralateral loss of pain and thermal sense on body (ALS)

• Ipsilateral loss of pain and thermal sense on face and in the
oral cavity (Spinal trigeminal tract/nucleus)
• Dysphagia , soft palate paralysis, hoarseness, diminished
gag reflex (Nucleus ambiguus, roots CNIX/X)

• Ipsilateral Horner syndrome ( miosis , ptosis, anhidrosis ,
flushing of face ) Hypothalamospinal fibers)

• Nausea , diplopia, tendency to fall to ipsilateral side,
nystagmus, vertigo (vestibular nuclei)

• Ataxia to the ipsilateral side ( restiform body, spinocerebellar
fibers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lateral Pontine Syndrome

A

Deficits: Contralateral loss of pain & thermal sensation (body)

Vascular Territory:
Occlusion of long circumferential branches of basilar artery and/or branches of anterior inferior cerebellar artery or superior cerebellar artery

Deficits vary depending on
whether the lesion is located
caudal or rostrally in the lateral
pons

(Have separate cards for different deficits based on structure damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Spinal Cord Injuries (SCI)

A

Spinal Cord Injuries (SCI) affect 250,000 450,000 people in the United States, most caused by trauma to vertebral column

Severity of an injury depends on the part of the spinal cord that is affected

Complete SCI produces bilateral, total loss of all motor & sensory function at/below the level of injury

Incomplete SCI, some function remains below the primary level of the

–> Anterior cord syndrome: injury to the motor & pain/temperature pathways in the anterior SC, patients still have proprioception & sensation

–> Central cord syndrome: damage to the center of the cord/AWC, causes loss of pain/temp pathways, with deficits relative to the size of the lesion

–> Injuries to a specific nerve root: may have motor & sensory deficits due to roots containing both types of nerves, and location of deficits depends distribution of nerve root involved

–> Spinal contusions: transient, generally resolving within 1 or 2 days; produce neurological symptoms including numbness, tingling, electric shock like sensations, & burning in the extremities. Chronic symptoms can take weeks to resolve.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is 2-point discrimination a diagnostic test for?

A

Diagnostic test for peripheral sensory deficiencies

Hypoaesthesia – abnormal sensory response in which sensation is reduced in one or more body parts in response to a stimulus such as touch, vibration or cold temperature. Partial numbness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Phantom Limb Pain

A

Pain in a body part that is no longer present
Occurs in many amputees

Law of Projection: No matter where along the afferent pathway a stimulation is applied, the perceived sensation arises from the origin of the sensation.
Stimulate along the same pathway (Peripheral nerve to spinal cord to primary and secondary cortex) & will think it’s from the thumb even if the thumb is not there.
Peripheral nerve still exists in brain and tries grow out to amputation area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lesions of the ALS:

A

Lesions of the ALS:

Blood supply originates from arterial vasocorona & via sulcal branches of the anterior spinal artery

Occlusion results in patchy loss of nociceptive, thermal,& touch over the contralateral side of the body, begins about two spinal segments below the lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Diagnostic test for peripheral nerve diseases

A

Interrelated classification (A, B, & C waves; Class I, II, III, & IV) because conduction velocity affects action potential & used as diagnostic test for peripheral nerve diseases (ex. Diabetic neuropathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is 2-point discrimination a diagnostic test for?

A

Hypoaesthesia – abnormal sensory response in which sensation is reduced in one or more body parts in response to a stimulus such as touch, vibration or cold temperature. Partial numbness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Phantom Limb Pain

A

Pain in a body part that is no longer present
Occurs in many amputees

Law of Projection: No matter where along the afferent pathway a stimulation is applied, the perceived sensation arises from the origin of the sensation.
Stimulate along the same pathway (Peripheral nerve to spinal cord to primary and secondary cortex) & will think it’s from the thumb even if the thumb is not there.
Peripheral nerve still exists in brain and tries grow out to amputation area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Asymbolia

A

pain is experienced without unpleasantness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Hyperaesthesia

A

Increased sensitivity to stimulation, excluding the special senses. Not increased pain, just increased sensitivity to a stimulus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

TRPA1 (Allyl isothiocyanate)

A

Involved in visceral pain; inflammatory pain states
Ex. allergic contact dermatitis, chronic itch, painful bladder syndrome, migraine, irritable bowel syndrome, and pancreatitis.

Anesthetics often have paradoxical pro-nociceptive effects by acting through TRPA1.

TRPA1 is an ion channel located on the plasma membrane of many human and animal cells. This ion channel is best known as a sensor for pain, cold and itch in humans and other mammals, as well as a sensor for environmental irritants giving rise to other protective responses (tears, airway resistance, and cough)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

TRPM8

A 
Cooling agents (ex. camphor or menthol - used for their analgesic properties)
Ex. topicals: Vicks Vaporub, Biofreeze, Oral-B oragel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Neurogenic inflammation

A

Neurogenic inflammation: proinflammatory signal from nociceptor (neuron) in periphery or brain.
In periphery, neurogenic inflammation due to hyperactive HPA (hypothalamic pituitary adrenal gland) access

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

TRPV1 (Vanilloid I)

A

Involved in chronic pain conditions (ex. migraine, dental pain, cancer pain, inflammatory pain, neuropathic pain, visceral pain, and osteoarthritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

TRPA1 (Allyl isothiocyanate)

A

Involved in visceral pain; inflammatory pain states
Ex. allergic contact dermatitis, chronic itch, painful bladder syndrome, migraine, irritable bowel syndrome, and pancreatitis.

Anesthetics often have paradoxical pro-nociceptive effects by acting through TRPA1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

TRPM8

A 
Cooling agents (ex. camphor or menthol - used for their analgesic properties)
Ex. topicals: Vicks Vaporub, Biofreeze, Oral-B orajel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Lateral Pontine Syndrome:

Structure damage:
Middle and superior cerebellar peduncles (caudal
and rostral levels)

What are the symptoms?

A

Occlusion of AICA

Ataxia, unsteady gait, fall toward side of lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Lateral Pontine Syndrome:

Structure damage: Vestibular and cochlear nerves and nuclei

What are the symptoms?

A

Vertigo, nausea, nystagmus, deafness, tinnitus,

vomiting (at caudal levels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Lateral Pontine Syndrome:

Structure damage: Facial motor nucleus (caudal levels)

A

Ipsilateral paralysis of facial muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Lateral Pontine Syndrome:

Structure damage: Trigeminal motor nucleus (midpontine levels)

A

Ipsilateral paralysis of masticatory muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Lateral Pontine Syndrome:

Structure damage: Descending
hypothalamospinal fibers

A

Ipsilateral Horner syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Lateral Pontine Syndrome:

Structure damage: Spinal trigeminal tract and nucleus

A

Ipsilateral loss of pain and thermal sense from

face

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Lateral Pontine Syndrome:

Structure damage: Anterolateral system

A

Contralateral loss of pain and thermal sense from

UE, trunk, and LE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Lateral Pontine Syndrome:

Structure damage: Paramedian
pontine reticular formation AKA PPRF (mid to caudal levels)

A

Paralysis

of conjugate horizontal gaze

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Onion-Peel Sensory Loss

A

Damage to spinal trigeminal tract yields onion peel sensory
loss:
• More caudal lesion → spares oral region, but affects posterior
& lateral boundaries of face
• More rostral lesion (into brainstem) → sensory loss that is increasingly anterior & converges on mouth

•Trigeminal fibers ending in the cervical cord
overlap spinal fibers that innervate C1, C2
dermatomes

• Allows for a smooth transition of cutaneous info
from posterior head (spinal) with cutaneous
anterior face/head (brainstem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Neurogenic inflammation

A

Neurogenic inflammation: proinflammatory signal from nociceptor (neuron) in periphery or brain.
In periphery, neurogenic inflammation due to hyperactive HPA (hypothalamic pituitary adrenal gland) access

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Damage to Insular Cortex

A

Damage causes asymbolia (noxious stimuli does not feel painful). Lesions in any single area alters the experience of pain but does not abolish it completely. Because pain is involved in so many regions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Minimally Conscious vs Persistent Vegetative State

A

Minimally conscious state: Cortex is active in minimally conscious state, sleep/wake cycles, reproducible evidence of awareness (ability to respond to simple commands), limited or absent communication

Persistent vegetative state: no evidence of awareness, physiologically identifiable sleep/wake cycles appear

in a persistent vegetative state, the rostral regions of the pons, midbrain, and thalamus show neuronal loss that exceeds that of the cortex

the RAS/parabrachial EAA system is crucial for increasing general excitability if cortical neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Ectopic Pituitary

A

low yield!!

Incomplete migration of hypophyseal diverticulum and neurohypophyseal diverticulum or have remnants => Pituitary agenesis.

Very rare, pituitary is in an adjacent sinus (sphenoidal, sella, hypoplastic posterior lobe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Damage to PPT/DLT

Cholinergic arousal system

A

Cholinergic role in arousal/awareness:

Activity in cholinergic inputs from the pons is also associated with arousal and awareness

Damage specifically to the PPT/DLT doesn’t necessarily cause coma, but does produce severe cognitive deficits that are associated with a generalized slowing of cortical processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What artery supplies the ventral posterolateral nucleus?

What would happen if these were occluded?

A

The thalamogeniculate branches of the posterior cerebral artery.

Lesions result in loss of all tactile sensation over the contralateral body & head

Usually both VPL and VPM affected due to their proximity

Vasculature lesions also link to deficits

Complete loss of discriminative touch, pressure sensation, and proprioception to the contralateral body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Effects of damage to primary afferents

A

Side affected: Ipsi
Strength: No change
Reflexes: Decrease/loss of function
Sensation: Decrease/loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What symptom is associated with damage to the secondary somatosensory area?

A

Agnosia – the loss of ability to recognize a limb as part of the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What artery supplies the ventral posterolateral nucleus?

What would happen if these were occluded?

A

The thalamogeniculate branches of the posterior cerebral artery.

Complete loss of discriminative touch, pressure sensation, and proprioception to the contralateral body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Effects of damage to primary afferents

A

Side affected: Ipsi
Strength: No change
Reflexes: Decrease/loss of function
Sensation: Decrease/loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Pharmacological intervention: Levadopa

A

in a limited number of people with persistent vegetative state, treatment with levodopa has produced dramatic increases in cognitive function

the dopaminergic system seems to add focused awareness associated with novel stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Effects of damage to Sensory Pathways (brainstem/2nd order neurons)

Effects of damage to PrimarySomatosensory (SI)Cortex

A

Side affected: Contra
Strength: No change
Reflexes: No change
Sensation: Loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Motor Reflexes in Brainstem/Midbrain: Suckle, Yawn, Eye/Head movements

A

These motor reflexes occur in anencephalic babies too (birth defect in which skull and membranes have failed to close and brain rostral to midbrain/some parts of midbrain have failed to develop).

These reflexes occur in absence of the cortex. SO anencephalic babies will move their heads/eyes towards motion/sound in absence of cortex. Looks like volitional activity but is not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Drug: Reserpine

A

VMAT2.

Reserpine inhibits this process. Leads to synaptic failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Serotonin receptor 5HT2c

A

knock-out mice are obese and seizure prone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Serotonin receptor 5HT3

A

located in area postrema –> induces vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Serotonin receptor 5HT6

A

anti-depressant effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Clinical relevance of Denate Nuclei

A

is a deep cerebellar nuclei

Dentate Nucleus
Gives rise to the vast majority of the efferents from the neocerebellum.

Dentate nucleus is mostly responsible for planning and execution of fine movement. There are several pathological disorders that may involve the dentate nucleus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Signs and symptoms of cerebellar dysfunction

A

Cerebellar: dysmetria (lack of coordination- undershoot or overshoot of movement), ataxia (mimics symptoms of being drunk), dysdiadochokinesia (not able to perform rapid movements), & intention tremor (amplitude of intention tremor increases as extremity approaches end of movement)

Additionally: Decomposition, slurred or scanning speech, rebound phenomenon, hypotonia & hyperflexia, & asthenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Ataxia- signs and symptoms of cerebellar dysfunction

A

Broad-based, staggering gait

note: think of ataxia as symptoms you’d have while drunk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Dysmetria- signs and symptoms of cerebellar dysfunction

A

Literally “missing the mark” during such tests as touching the fingertip to the nose with the eyes closed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Dysdiadochokinesia- signs and symptoms of cerebellar dysfunction

A

Inability to perform rapidly alternating movements such as pronation and supination.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Intention Tremor-signs and symptoms of cerebellar dysfunction

A

Tremor is usually characteristic of lesions involving the superior cerebellar peduncle or dentate nucleus. It is present during voluntary movements such as reaching for a pencil on a table, and absent during rest. As the patient reaches for the object, the tremor (actually an escalating series of gross over compensations) progressively worsens.

62
Q

Decomposition of Movement- signs and symptoms of cerebellar dysfunction

A

Some patients with cerebellar dysfunction may exhibit a breakdown of the fluid, multi-joint patterns of movement. Movements tend to be performed one joint at a time, and take on a “robotic” appearance.

63
Q

Slurred or Scanning Speech-signs and symptoms of cerebellar dysfunction

A

It is not unusual to witness this speech pattern in alcohol intoxicated individuals. Alcohol, as well as cerebellar disorders, affects an individual’s ability to coordinate the complex motor speech patterns involved in vocalization.

64
Q

Rebound Phenomenon-signs and symptoms of cerebellar dysfunction

A

Inability of opposing muscles to stop an action, e.g., bicep curl

65
Q

Hypotonia and Hyporeflexia-signs and symptoms of cerebellar dysfunction

A

Hypotonia is the medical term for decreased muscle tone. Healthy muscles are never fully relaxed. They retain a certain amount of tension and stiffness (muscle tone) that can be felt as resistance to movement.

Hyporeflexia refers to a condition in which your muscles are less responsive to stimuli. If your muscles don’t respond at all to stimuli, this is known as areflexia. Your muscles may be so weak that you can’t do everyday activities.

66
Q

Asthenia-signs and symptoms of cerebellar dysfunction

A

The patient may demonstrate weakness of the limb or axial musculature.

67
Q

Nystagmus-signs and symptoms of cerebellar dysfunction

A

Lesions of the vestibulocerebellum may result in nystagmus.

Irregular movements of the eye

68
Q

Alcohol Degeneration of the Cerebellum

A

Chronic indigestion of ethanol causes a cortical atrophy of the anterior lobe of the cerebellum, and (in advanced cases) the neocerebellum and dentate nucleus.

Late stages of the disease: patient presents with severe ataxia of the lower extremities and trunk, and a relatively minor involvement of the upper limbs.

The disease may be seen in conjunction with other conditions such as Korsakoff’s syndrome.

Alcoholic cerebellar degeneration caused by its direct toxic effect to the cerebellum and the consequences of vitamin B1 (thiamine) deficiency. Alcohol also produces a toxic effect on Purkinje cells.

69
Q

Ipsilateral cerebellar lesion:

A

Ipsilateral cerebellar lesion: Positive heel to shin test (abnormal if there is loss of motor strength, proprioception or a cerebellar lesion. If motor and sensory systems are intact, an abnormal, asymmetric heel to shin test is highly suggestive of an ipsilateral cerebellar lesion.)

70
Q

Friedreich’s Ataxia

A

is an autosomal recessive degenerative disease of adolescence and early adulthood. It involves a progressive neuronal necrosis and resultant demyelination of the proprioceptive neurons in the dorsal roots, posterior columns, medial lemniscus, spinocerebellar tracts, and corticospinal tracts, in addition to the degeneration of the Purkinje cells, dentate nucleus and superior cerebellar peduncles. Cardiac hypertrophy and diffuse myocardial fibrosis are also present.

The ataxia initially develops in the lower limbs and progresses to the upper limbs over the course of a few years.

Dysdiadochokinesia, dysmetria, nystagmus and intention tremor are all present bilaterally.

The patient exhibits a wide-based gait with severe ataxia and some degree of spasticity.

Optic atrophy, hearing loss, dysarthric speech (slow, staccato and explosive) as well as dementia may eventually develop. Death occurs 10 to 20 years after onset from cardiac or pulmonary complications.

71
Q

What neurons are primarily destroyed in Parkinson’s Disease?

A

Neurons in the pars compacta (of the substantia nigra) contain dopamine and melanin.
CLINICAL: neurons in the pars compacta are principally destroyed in Parkinson’s disease.

72
Q

Unilateral lesion of the red nucleus and midbrain tegmentum, such as in Benedikt’s syndrome

A

Red nucleus is associated with basal ganglia

Patients, who have a unilateral lesion of the red nucleus and midbrain tegmentum, such as in Benedikt’s syndrome, present with ipsilateral oculomotor palsy, and contralateral motor dysfunction such as tremor, ataxia or choreiform movements.The contralateral abnormal involuntary motor movements are probably due to the involvement of the crossed fibers of the superior cerebellar
peduncle that course through and around the red nucleus.

73
Q

Unilateral Lesions of subthalamus

A

Unilateral lesions of the subthalamus result in hemiballismus

74
Q

Huntington’s Chorea

A

Striatonigral fibers:
GABAnergic fibers

Destruction of the inhibitory, GABA-nergic fibers in the striatonigral fibers are involved in Huntington’s chorea

Autosomal dominant motor disorder, localized on the short arm of chromosome 4.

Common features include dementia, chorea and behavioral disturbances.

  • ->Choreiform movements are characterized by sudden, irregular, involuntary, jerky, purposeless movements.
  • ->May develop severe dementia.
  • ->An athetosis component (choreoathetosis) may be present

Principal areas of degeneration are the corpus striatum and the cerebral cortex.

Symptoms may be due to excessive dopaminergic influence in the degenerated striatum or loss of inhibition from the GABA-nergic neurons of the striatonigral pathway.

75
Q

Parkinson’s Disease:

A

Nigrostriatal Fibers: dopaminergic fibers that originate in the pars compacta of the substantia nigra, and terminate in the caudate and putamen (striatum).
–> The neurons in this area of the substantia nigra are destroyed in Parkinson’s disease.

Dopaminergic Fibers

Nigrothalamic fibers are non-dopaminergic fibers that originate from the pars reticularis of the substantia nigra and terminate in the VA and VL thalamic nuclei.

Fibers from the globus pallidus and the substantia nigra do not terminate in the same areas of the VL and VA thalamic nuclei. This distinction was important in stereotaxic surgery for Parkinson’s disease

76
Q

Hemiballiam

A

Unilateral lesions of the subthalamus or its connections result in contralateral hemiballism, characterized by violent, involuntary, flinging movements of the limbs (upper and lower).

These movements usually involve muscles of the shoulder and hip regions, and proximal limb musculature. It is always associated with hypotonus.

The subthalamic nucleus (STN) receives major input from the globus pallidus (lateral portion) and motor cortex. Subthalamic neurons contain glutamate and exert an excitatory influence.

These movements may be due to a reduction or loss of inhibition on the globus pallidus by the subthalamus. It is an example of a release phenomenon. Symptoms can decrease during sleep.

77
Q

Athetosis

A

Sign & Symptoms: Slow, involuntary, writhing movements of the limbs & face.

Due to: Degeneration of the striatum.

78
Q

Dystonia:

A

Dystonia is a movement disorder in which a person’s muscles contract uncontrollably. The contraction causes the affected body part to twist involuntarily, resulting in repetitive movements or abnormal postures. Dystonia can affect one muscle, a muscle group, or the entire body.

Dystonia is a sustained or repetitive muscle twisting, spasm or cramp that can occur at different times of day and in different stages of Parkinson’s disease (PD). For example, dystonia is a common early symptom of young-onset Parkinson’s.

79
Q

Acute Poliomyelitis:

A

Acute anterior poliomyelitis selectively involves the motor neurons of the anterior horns and the cranial nerve motor nuclei.

Initially, there is often severe inflammation, vasodilation, edema, and macrophagic activity. Subsequently, these neurons die and there is significant astrocytic gliosis.

80
Q

Lower Motor Neuron Paralysis

A

Lower motor neuron (LMN) paralysis results from the destruction of the motor neurons or the axons of one or more of the cranial or spinal motor nuclei.

Signs and symptoms of lower motor neuron lesions include: flaccid paralysis, areflexia, atonia, atrophy, and fasciculations.

Lesions of the ventral roots (anterior horn) causes a lower motor neuron (LMN) paralysis of the associated motor dermatome: atonia, areflexia, fasciculation, and flaccid paralysis.

Poliomyelitis
ALS

81
Q

Upper Motor Neurons Paralysis

A

Lesions of the motor cortex, corticospinal and/or corticobulbar tracts result in an upper motor neuron (UMN) paralysis.

UMN paralysis is referred to as spastic paralysis of the antigravity muscles, which is characterized by hypertonia, hyperreflexia, Babinski sign, clonus (involuntary muscle contractions), and disuse atrophy.

The corticospinal tract are upper motor neurons (UMN). A lesion of the CST results in contralateral spastic hemiplegia: hyperreflexia, hypertonia, paralysis and disuse atrophy

Spastic paralysis is most pronounced in the distal limb musculature, especially of the upper extremity. However, other descending tracts are usually involved and probably contribute to the overall motor findings. [Although rare, pure isolated lesions of the corticospinal tract result in paresis and incoordination of primarily the distal musculature of the extremities.

Sign & Symptoms:
Spastic paralysis
–>Hypertonia, Hyperreflexia, Babinski sign, Clonus

Caused by:
Spinal Cord transection
ALS

82
Q

Amyotrophic Lateral Sclerosis (ALS) AKA Lou Gehrig’s Disease

A

Cause is unknown, may be due to defect in glutamate metabolism

Average age of onset is 66

Most common form of ALS involves combo of these structures:

  • ->LMN: Anterior horn cells, Hypoglossal nucleus, Nucleus ambiguus, Facial motor nucleus
  • ->UMN: Chronic, progressive degeneration of the corticospinal tracts

ALS leads to LMN paresis and atrophy of the intrinsic muscles of the hands followed later by the arms and shoulder musculature. Patients may develop dysarthria, dysphagia and paresis of the tongue.

Involvement of the CST leads to spastic paralysis, hyperreflexia and a Babinski sign.

There are no sensory deficits associated with ALS, although the patient
may have sensory deficits related to another disease process, e.g., diabetic neuropathy.

Death is due to bulbar paralysis, i.e., the vital respiratory centers, within an average of four years of onset.

83
Q

Parkinson’s Disease

A

Subcortical degeneration disorder involving the substantia nigra, globus pallidus, upper brainstem nuclei (mainly RF), and occasionally the postganglionic sympathetic neurons.

Major causes: postencephalitic, arteriosclerotic, and drug-induced.

Signs and symptoms of PD: bradykinesia (slow movement), tremor during rest (can be heightened by emotions), rigidity, masked face and positive Glabellar sign (aka tapping on forehead will result in no blinking), and postural embarrassment (early cases involve short, choppy steps and more severe cases have severe postural embarrassment)

84
Q

Tardive Dyskinesia

A

Caused by over use of neuroleptic medications. Tardive dyskinesia is characterized by repetitive involuntary licking and smacking movements of the lips.

May result primarily from neuroleptic-induced dopamine supersensitivity in the nigrostriatal pathway, with the D2 dopamine receptor being most affected.

Neuroleptics act on this dopamine system

Older neuroleptics, which have greater affinity for the D2 binding site, are associated with high risk for tardive dyskinesia.

85
Q

Globus Pallidus Syndrome:

A

Hypobaric hypoxia at high elevation induced this neurobehavioral syndrome.

  • -> Apathy
  • -> Lack of motivation

Clinically indistinguishable from a frontal lobe syndrome.

Lesions of subcortical structures may cause executive dysfunction.

Bilateral hemorrhages of globus pallidus. Similar to bilateral frontal lobe disease.

86
Q

Expressive or Broca’s Aphasia

A

A lesion of Broca’s speech area in the dominant hemisphere results in expressive or nonfluent motor aphasia. Aphasia is a true language disturbance in which there are errors in grammar and word choice.

The basic defect is in higher integrative language processing as a result of brain damage.

The patient with motor aphasia is unable to speak fluently, because he cannot select the appropriate grammar and/or words.

87
Q

Spastic hemiplegia

A

indicates involvement of corticospinal tract.

88
Q

Apraxia

Ideomotor apraxia

Ideational apraxia

A

Apraxia:is the inability to perform certain complex learned motor acts in the absence of any paralysis, ataxia, sensory changes, or deficiencies of understanding (confusion). Patient cannot perform the motor sequence correctly although they know the position of their limb. Often due to lesion in superior parietal lobe of dominant hemisphere.

Two types
Ideomotor apraxia is the inability to perform a given act correctly although old, habitual motor acts can be performed spontaneously or repetitiously (often with perseveration). Associated with lesions of the supramarginal gyrus of the dominant hemisphere.

Ideational apraxia is a loss of the ability to formulate the ideational concepts necessary to perform a motor activity. The patient can perform the isolated tasks, but not a series of related tasks. Occurs because of brain disorders such as cerebral arteriosclerosis. This type of apraxia is seen with widespread intellectual deterioration. (Example: may be hard/impossible to fold letters, put in envelope, seal, etc.)

Note: The supramarginal gyrus (plural: supramarginal gyri) is a portion of the parietal lobe of the brain. It is one of the two parts of the inferior parietal lobule, the other being the angular gyrus. It plays a role in phonological processing (i.e. of spoken and written language) and emotional responses.

89
Q

Agnosia:

A

inability to interpret sensations and hence to recognize things, typically as a result of brain damage.

left-right disorientation (ex: patient will raise his right hand but tell you they are raising left). However, Automatic voluntary dissociation is still present (aka patient will still pick up pencil with dominant right hand)

90
Q

Requirement for Neurological exam

A

patient needs to be able to sense, understand (language), and comprehend commands. Patient needs attention and motivation to perform on the exam.

Attention (frontal lobe)

  • Prefrontal lobe: motivation (nucleus accumbens, amygdala, and olfactory tubercle) and memory.
  • Deficit leads to apathetic, and difficult to test patients for any cognitive activity. Elicit volitional movements or remember how to perform a movement.

__________________________________

Note: The nucleus accumbens definitely plays a central role in the reward circuit. Its operation is based chiefly on two essential neurotransmitters: dopamine, which promotes desire, and serotonin, whose effects include satiety and inhibition.

91
Q

standing (Romberg test)

A

A positive Romberg test indicates ataxia from dorsal column disease and impaired proprioception. Normally, vision will compensate for the sensory loss. Cerebellar and vestibular disease is indicated if patient cannot stand with their feet together regardless if their eyes are open or closed

92
Q

Ideomotor apraxia (IMA)

A

is the inability to correctly imitate hand gestures and mime tool use (ex: pretend to brush own hair). The left parietal lobe and the premotor cortex are frequent sites of lesions that result in ideomotor apraxia. Note: In the dominant hemisphere, aphasia (can’t understand or express speech) is often present

93
Q

Aphonia

A

loss of ability to speak through disease of or damage to the larynx or mouth.

94
Q

Encephalization

A

The primary motor cortex exerts a dominant influence over subcortical systems. The close relationship between the POT & primary motor cortex in the dominant requires the examiner to assure the patient’s ability to comprehend the verbal command. The patient may have receptive aphasia.

Higher degrees of encephalization are generally correlated with higher degrees of intelligence

95
Q

[Pyramidal System] Lenticulostriate infarcts

A

Lenticulostriate infarcts (tissue death or necrosis due to inadequate blood supply → resulting lesion is called infarct): Result from ischemia within the territory supplied by perforating branches of MCA (supplies the primary motor and primary somatosensory cortex) or ICA. Signs include motor and/or sensory deficits and cognitive dysfunction

96
Q

unilateral lesions of the anterior corticospinal tracts (ACT)

A

have minimal clinical effect

97
Q

Absence of descending tract influence on LMN

A

descending tracts help to excite or inhibit LMN’s. Absence of descending tract influence on LMN is seen in many motor system disorders. Example: Parkinson’s, rigidity, spasticity, hemiballismus (basal ganglia syndrome, damage to the subthalamic nucleus-> violent involuntary movements)

98
Q

Unilateral Lesions of CST

A

result in contralateral spastic hemiplagia or spastic hemiparesis

spastic hemiparesis, means that one half of the body is afflicted with weakness, but is not paralyzed

Spastic hemiplegia is a neuromuscular condition of spasticity that results in the muscles on one side of the body being in a constant state of contraction

99
Q

Unilateral lesions of the LCST

A

result in paralysis or paresis of the distal limb muscles below the level of the lesion.

(ipsilateral or contralateral depends on location of lesion)

100
Q

Lesions of a LMN result in (5 things)

A
  1. Flaccid paralysis. Muscle is completely “limp” and there is no resistance to passive movement (because LMN that goes to muscle is damaged, so muscle contraction not possible)
  2. Areflexia. The loss of the efferent component of the reflex arc to a muscle results in the an absence of the associated muscle reflex
  3. Atonia. Destruction of gamma motor neurons or their axons results in the absence of muscle tone
  4. Atrophy. Denervated muscle atrophies due to the loss of stimulation from the motor neurons
  5. Fasciculations or twitching” of the denervated muscle, probably due to hypersensitivity of the motor end plate
101
Q

Lower Motor Neuron Signs

A

● Flaccid paralysis
○ Destruction of the final common pathway
● Muscle wasting
● Hyporeflexia / areflexia
● Hypotonia
● Denervation hypersensitivity and fasciculations.
○ This is due to acetylcholine entering the synapse at random after the death of the lower motor neuron.

102
Q

Upper Motor Neuron Signs

A

AKA Spastic paralysis: commonly due to interruption of motor cortex, corticospinal and/or corticobulbar tracts.
● spastic paresis of the axial and proximal (some distal) limb musculature, esp upper extremity
● Hypertonia, babinski sign, disuse atrophy,
● Loss of distal strength and dexterity as well as Babinski sign (inverted plantar reflex).
○ Both of these are due to a direct loss of the corticospinal tract.
● Spasticity
○ Rate dependent resistance to passive movement with a “clasp knife” like release of resistance at the end of the range of motion.
● Rigidity
○ Constant resistance throughout range of motion.
○ Associated with basal ganglia disease.
● Hyperreflexia (possibly with clonus)
● Pronator drift

103
Q

Lesions of Corticobulbar Tract:

A

Unilateral lesions of the CBT above the decussation (un-crossed) may result in some contralateral cranial nerve palsies (see supranuclear facial palsy). Unilateral lesions below the decussation may cause ipsilateral cranial nerve palsies. Later, many of these deficits are improved due to the varying degree of bilateral innervation of the nuclei as well as the neuronal plasticity of the reticular formation and the corticoreticulobulbar fibers.

104
Q

Indirect Corticobulbar fibers (aka corticoreticulobulbar fibers)

A

do not affect the LMN’s as much as direct corticobulbar fibers; play a role in the recovery from lesions involving the direct corticobulbar fibers, and have a role in physical therapy.

105
Q

Supranuclear Facial Palsy

A

Unilateral lesions of the CBT above the decussation (un-crossed) result in contralateral supranuclear facial palsy. Refers to paralysis of the contralateral (from the corticobulbar fiber lesion) mimetic (muscles innervated by the facial n.) muscles on the lower quadrant of the face are paralyzed. Upper quadrant of face is unaffected. Most common site of lesions causing this are the facial region of the motor cortex and genu of internal capsule.

106
Q

Corticomesencephalic fibers

A

The separation of these fibers from the corticospinal and corticobulbar fibers makes it difficult to destroy all three in the same lesion

107
Q

Decorticate posturing

A 
o UMN lesion 
▪ Rigidity 
• Lesion above red nucleus: above midbrain 
• Thumb tucked under flexed fingers in fisted  
position 
• Pronated forearm 
• Flexion at elbow 
• LE in extension with foot inversion

Decorticate posture
•Internal rotation of legs in extended position; flexion of arms; dependent on head position.
•May be bilateral or unilateral.
•Loss of cortical inputs – most commonly caused by lesion of internal capsule in humans.

whatever side you turn your head to, that arm will be more flexed

108
Q

Decerebrate posturing

A

o UMN lesion
▪ Lesion below the red nucleus but above reticulospinal and vestibulospinal nuclei
▪ UE pronation and extension
▪ LE extension

•Decerebrate posture
•Contraction of all anti-gravity muscles (arms in extension)
•Loss of input from all structures rostral to the pons (caudal to red nucleus).
•Usually indicative of severe brain injury.
Can have some axonal recovery

109
Q

Complete transection of the spinal cord

A 
o All sensation of 1 or 2 levels below lesion 
o Bladder and bowel control lost 
o Spinal shock 
▪ Loss of tendon reflexes 
o UMN signs at levels below lesion 
▪ Hyperactive reflexes, clonus  
▪ Babinski 
▪ Spasticity  
o LMN signs at level of lesion
110
Q

Syringomyelia

A 
o Most often at C4/5 but can also occur at other levels,  associated with Chiari Type 1 
o Formation of cyst within SC 
o Pain and temp 1st affected 
▪ Anterior white commissure 
▪ Resulting pattern is cape shaped 
o Motor lost

Note: Important assessment for Chiari malformations is to view a sagittal MRI section to observe the relationship of the (cerebellar) Tonsils to the Foramen magnum. Ps. check the upper cervical cord for a syrinx.

111
Q

amyotrophic lateral sclerosis (ALS)

A

• Destroys somatc motor neurons
o UMNs, brainstem, and SC LMNs
• Leads to paresis, myoplastic hyper stiffness, hyperreflexia, Babinski, atrophy, fasciculations, fibrillations
• CN involvement leads to difficulty breathing, swallowing, and speaking

112
Q

Central Seven Palsy

A

o Lesion of corticobulbar tract involving CN VII
o Muscles of upper face are controlled by equal number of fibers from both hemispheres
o Muscles of lower face are controlled by contralateral hemisphere
o Lesion rostral to facial motor nucleus results in drooping of muscles at corner of mouth
▪ On OPPOSITE side of lesion

113
Q

Bell’s Palsy

A

o Ipsilateral flaccid paralysis of upper and lower face

114
Q

The lenticulostriate arteries(of the MCA) supply most of the internal capsule

A

• So you would find the following deficits:
o Weakness of the face, arm, and/or leg
o Hyperreflexia
o Babinski sign
o Clonus
o Spasticity
o Contralateral weakness and sensory loss

115
Q

Spinal shock

A

The term “spinal shock” applies to all phenomena surrounding physiologic or anatomic transection of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity below the level of the injury.

A spinal cord transection causes a bilateral loss of all myotatic reflexes below the site of transection. All reflexes abolished, even if circuit is intact

Recovery of reflexes is believed to result from:
•Axonal sprouting below the level of the transection. •Expression of receptor phenotypes that are self-activating (5HTC receptor - Ionotropic
Creates na channel that can open on its own, in addition to serotonin released from some of the axonal sprouting.)

•Cause: hyperpolarization of spinal neurons due to loss of excitatory input from cortex? Alpha motor neurons too far from threshold for excitation, so need background excitation.

116
Q

Spasticity

A
  • Patient resists a passive stretch of their muscles
  • The contraction doesn’t start until the stretch occurs
  • Hyperactive myotaticreflex due to increased gamma motoneuronfiring.

•Cause: damage to cortex that abolishes activation of the brainstem inhibitory region (brain arousal systems)

Spasticity is a condition in which muscles stiffen or tighten, preventing normal fluid movement. The muscles remain contracted and resist being stretched, thus affecting movement, speech and gait.

117
Q

Rigidity

decorticate posturing

A
  • Contraction of muscles in the absence of other stimuli. •Alpha-moto neurons continually active
  • Cause: Loss of cortical influence that inhibits a medullary input to the alpha-motoneurons

Upper midbrain damage

Decorticate posturing (rigidity)
•Flexion of the upper limb joints (disinhibition of red nucleus & its control of UE flexors).
•Extension of the lower limbs (disinhibition of reticulospinal and vestibulospinal pathways)
•Dependent on head position (release of postural reflexes)

You are extremely likely to see patients with unilateral decorticate posturing.
•results from strokes in the vicinity of the internal capsule
•a relatively common site for a stroke.

118
Q

Brainstem facilitatory region

Brainstem inhibitory region

A

Brainstem facilitatory region
•by activating the gamma-motoneurons, makes muscle spindle more sensitive.
•This region is spontaneously active.

Brainstem inhibitory region
•inhibits gamma motoneurons, making muscle spindle less sensitive.
•This region requires activation from cortical regions.

With the loss of the cortex, the brainstem (-) region is not activated, leaving the(+) region to dominate. –> Hyperactive reflex, Spasticity

119
Q

In Parkinson’s Disease the substania nigra pars compacta input is abolished. What are the 2 effects?

A
  1. The direct pathway becomes difficult to activate.
  2. The indirect pathways becomes overactive (due to loss of inhibition)

Therefore we see an inability to initiate motion.

120
Q

Doll Eye’s Maneuver

A.Right III palsy: when turning pt’s head to R, their R eye is neutral and L abducts

B.Left III palsy: when turning pt’s head L, their L eye is neutral and R abducts

C.Right VI palsy: when turning pt’s head to left, their L eye adducts and R is neutral

D.Left VI palsy: when turning pt’s head to R, their R eye adducts and L is neutral

A

The eyes will continue to look straight forward as the head is turned side to side. This tests the neuronal link between the vestibular nuclei and the system that controls horizontal gaze. Normal response to align body with eyes. In the unconscious patient without cervical injury, side-to-side movement of the head results in horizontal movement of the eyes in the opposite direction.

Note: Perform a GCS evaluation to assess the level of consciousness. A routine neuro exam and/or a MMSE are not possible in an obtunded patient. The Doll’s eyes maneuver is CONTRAINDICATED in a patient with suspected or confirmed C-spine injury. After the patient is stabilized, the neurosurgical consult is usually appropriate.

121
Q

Oculocaloric Testing for Vestibuloocular Response (VOR)

**refer to table in Vestibular System Summary Sheet!

A

● (COWS is the mnemonic for the direction of nystagmus (involuntary eye movements): (COWS- cold opposite; warm same)
● Intact brainstem: ice water caloric testing causes the eyes to turn toward the stimulus and they show horizontal nystagmus to the non-stimulated (opposite) ear
● Warm water caloric testing normally causes the eyes to turn away from the stimulus with horizontal nystagmus toward the stimulated ear. Absent VOR suggests ipsilateral vestibular impairment of the stimulated lateral semicircular duct.
● Comatose patient with cerebral damage: Cold water irrigation causes deviation of the eyes toward the ear being irrigated. If responses are bilaterally absent and there is no nystagmus, this indicates midbrain damage and a poor prognosis

122
Q

Unilateral Lesions of the Vestibular System

A

Unilateral lesions of the vestibular system cause ipsilateral signs and symptoms
● Has nausea, vomiting, postural impairment, nystagmus
● Nystagmus is described according to the fast component, which is directed toward the side of the lesion.11
● Vertigo: Generally, the dizziness is in the same direction as the slow component of the nystagmus (opposite the lesion).12
● Postural impairment is assessed using the Romberg test. The normal function of the posterior columns (proprioception), vestibular system, and vision is necessary to maintain balance while standing. The patient is usually tested standing, with feet together, and then closing his eyes for one minute. The examiner should stand near the patient in case of a fall.
● Romberg test: If a standing patient with his eyes closed sways or falls during the Romberg test, it is a positive Romberg test, and a type of sensory ataxia. If a patient is ataxic and Romberg’s test is normal, it suggests cerebellar ataxia.
● Patient tends to fall toward the side of the lesion. Midline lesions of the cerebellum, especially the nodulus (vestibulocerebellum) cause truncal ataxia and postural imbalance.
● Eyes, head and body tend to turn toward the side of the lesion
● Visceral disturbances such as nausea, vomiting, and pallor.
● Many of these vestibular deficits will attenuate with time due to the compensation of the visual and general proprioceptive systems.

123
Q

Nystagmus

A

Nystagmus may be caused by congenital disorders, acquired or CNS disorders, toxicity, pharmaceutical drugs, alcohol, or rotational movement. It may be associated with vertigo

124
Q

Vertigo

A

: Benign paroxysmal positional vertigo (BPPV), Ménière’s disease, and labyrinthitis commonly cause vertigo. Vertigo may also be present secondary to stroke, brain tumors, brain trauma, MS, migraines ears or vestibular dysfunction. Physiologic vertigo is a transient episode due to excessive motion of the head

125
Q

Lesions of the Medial Longitudinal Fasciculus

Hint:
Right, right, right
Left, left, left

Right INO=right MLF lesion→right CN III impaired

Left INO=left MLF lesion→left CN III impaired

A

: A unilateral lesion of the MLF superior to the abducens nucleus results in a contralateral disturbance of horizontal gaze (impairment of adduction (MR) of the ipsilateral eye and nystagmus of the abducting eye).
If the lesion is of the right MLF, horizontal gaze to the right is normal.
● Horizontal gaze to the left exhibits paresis of the adductor (medial rectus) of the right eye, and nystagmus of the left (abducting) eye.
● This is referred to as a right Internuclear ophthalmoplegia.(INO)
● INO is named according to the side of the oculomotor impairment

EX: Right INO –> Right MLF damage –> Right eye cannot adduct, left eye has nystagmus

126
Q

Clinically Isolated Syndrome:

A

: CIS is a first episode of neurologic symptoms caused by inflammation and demyelination in the CNS. Patients, who experience CIS, may or may not develop MS. When CIS is accompanied by sclerotic lesions on MRI, a second episode of neurologic symptoms and diagnosis of relapsing- remitting MS is probable.

Neuromyelitis optica (NMO; Devic disease or Devic syndrome) is a CNS demyelinating with clinical manifestations similar to those of MS. Patients have one or more clinical episodes of optic neuritis along with myelitis. Although these events are frequently found in typical MS, in NMO they are usually more acute and severe.

127
Q

Vestibular Dysfunction

A

Unilateral lesions of the vestibular system manifest their signs and symptoms ipsilaterally. Many vestibular deficits will attenuate with time due to the compensation of the visual and general proprioceptive systems.
● Ipsilateral postural impairment (positive Romberg’s test)
● Vertigo: Generally, The dizziness is in the same direction as the slow component of the nystagmus (opposite the lesion).
● Nystagmus is described according to the fast component, which is directed toward the side of the lesion. Lesions of the vestibulocerebellum may result in nystagmus.
● Visceral disturbances such as nausea, vomiting, and pallor.
● Eyes, head and body tend to turn towards the side of the lesion
● Patient tends to fall towards the side of the lesion

128
Q

Medulloblastoma

A

LOOK UP or fill in after looking at cases in lecture

Google says:

Medulloblastoma (muh-dul-o-blas-TOE-muh) is a cancerous (malignant) brain tumor that starts in the lower back part of the brain, called the cerebellum. The cerebellum is involved in muscle coordination, balance and movement.

129
Q

Tumor of the Fourth Ventricle:

A

Tumors of the posterior cranial fossa are more common in children, and in this case a midline tumor has damaged the vestibular area of the rhomboid fossa and the adjacent flocculo-nodular lobe of the cerebellum. Lesions of the vestibular system tend to manifest their signs on axial (or postural) musculature and the oculomotor system (nystagmus).

130
Q

Unilateral PPRF Lesion:

A

A unilateral lesion of the PPRF results in paresis or paralysis of horizontal gaze toward the same side of the lesion, and a gaze preference away from the side of the lesion. This deficit is due to the destruction of fibers that course from the PPRF to the ipsilateral abducens nucleus and contralateral oculomotor nucleus.

For example, a lesion of the right PPRF would result in the patient’s inability to move both eyes in conjugate horizontal gaze to the right. Their gaze preference would be to the left.

131
Q

Horizontal gaze

A

The Doll’s eyes maneuver and ice water oculocaloric testing are vestibulo-ocular responses that use the MLF. Horizontal gaze to either side is controlled by the contralateral MLF.

132
Q

Reticular Formation

A

Vestibular nuclei have bilateral projections into the reticular formation. These connections affect the somatic motor system (postural tone), and provide a mechanism for the visceral autonomic disturbances associated with vestibular stimulation (pallor, nausea, vertigo, vomiting, etc.).

133
Q

SEROTONIN (5HT) Receptors

A
  • 5HT2c: knock-out mice are obese & seizure prone
  • 5HT3: area postrema(vomiting)***
  • 5HT6: anti-depressant effect***
  • 5HT7: limbic system (mood)
134
Q

Histamine Receptors

A

•3 receptor types
• Serpentine receptors
• H1: PLC activation (Gq/11 protein)
• H2: ↑cAMP(associated with gastric acid release, Gs. Meds like pepto block H2 receptor)
• H3: presynaptic, decrease histamine release
• More H1 and H3 in brain than H2
• H1 involved in wakefulness
Less H2 because H2 is for releasing stomach acid.

Anti-histamine are nondrowsy, block H1

135
Q

GABA A receptors

A
  • Ionotropic (Cl conductance) •Activation produces ipspin adult neurons.
  • Multiple binding sites modulate:
  • Benzodiazepine site (increase Cl- coming through)
  • Ethanol
  • Certain steroids
  • These all potentiate.

increase IPSP

136
Q

Extra-synaptic GABA A receptors

A

It appears that there are a large number of extra-synaptic GABA A receptors. These receptors are believed to be the site of action for a number of general anesthetics, including propofol.

137
Q

Glycine Receptor

A 
Receptor
•Ionotropic (Chloride)
•Influx of chloride leads to ipsp.  
•Ethanol & general anesthetics bind to it and potentiate.  
•Strychnine binds to it and blocks it
138
Q

PEPTIDE TRANSMITTERS

These neurotransmitters are peptides made in the soma and transported down the axon via fast axonal transport.

A

Includes several transmitters: •The opioids (the only ones we’ll talk about)
•The tachykinins, including Substance P (Sensory innervation of cerebral vasculature; Dilator.)
•Cholecystokinin (A hormone in the gut that causes gall bladder contraction, it is also a neurotransmitter/neuromodulator at some synapses)
•Somatostatin (inhibits growth hormone effects, also inhibits at synapses)

139
Q

What are the 4 opioids (family of peptides)?

A
  • The endorphins(endogenous morphines– we knew about morphine first).
  • The enkephalins
  • The dynorphins
  • Nociceptin
140
Q

Fxn of Opioids

A
  • General Functions
  • Modification of nociceptive inputs (Cutaneous senses). •Mood/Affect (Neurophysiology of Emotion/Drug Addiction)

Mood (pleasure), Modifying Nociperception inputs.
Basal ganglia projections to multiple pontine & medullary sites.

141
Q

Opioid Receptors

  • Mu
  • Kappa
  • Delta
A
  • All opioid receptors are metabotropic (serpentine) and activate second messenger systems with ligand binding.
  • All connect to Gi/Go proteins
  • Mu receptor: leads to an increase in potassium efflux and hyperpolarization.
  • Delta- and Kappa-receptors: •Decrease calcium influx.
μ– Receptors (Mu)
•Metobotropicreceptor
Activation causes: 
•Analgesia
•Respiratory depression
•Euphoria
•Constipation
•Sedation
  • Kappa (К) receptors
  • Serpentine
  • Produces
  • Analgesia***
  • Dysphoria***
  • Diuresis
  • Miosis
  • Delta (δ) receptor
  • Serpentine
  • Produces analgesia when activated.
142
Q

Exo- & Endogenous Endocannabinoids

A

Exogenous chemicals (THC –Δ9-Tetrahydrocannabinol).

Endogenous cannabinoids are:
Anandamide
2-Arachidonylglycerol (2AG)

143
Q

Endocannabinoid Fxns based on brain region

A
  • Broadly distributed in the CNS
  • Basal ganglia•Mood•Motor performance
  • Spinal cord•Modulation of nociception
  • Cortex•Neuroprotection
  • Hippocampus•Memory formation
  • Hypothalamus •Control of body energy/hunger
144
Q

2-AG is major source for Arachidonic acid in certain tissues, especially brain.

A

•Consequence: Pharmacologic manipulation of 2-AG production has wide reaching effects beyond those of the endocannabinoid system.

145
Q

Cannabinoid Receptor #1

A

o Neuronal location
oActivation associated with the psychoactive responses to the cannabinoids
oIn humans, 472 amino acid peptide coupled to G-proteins. o97-99% homology with the mouse and rat versions of the receptor. oLocated on chromosome 6
oPolymorphisms linked to occurrence of obesity, ADHD, schizophrenia, and depression in Parkinson’s disease.
oCan form a heterodimer with other NT receptors, including dopamineand orexin.

146
Q

CANNABINOID RECEPTORS –CB2

A
  • Were initially reported as peripheral receptors, found primarily on macrophages
  • More detailed studies do find them in the brain, but on the microglia. •Neuronal location (dendrites and within soma) are also reported, usually associated with nerve injury. •Highly inducible in response to injury or inflammation. •Binds 2-AG better than AEA.
147
Q

The NMDA (N-methyl-D- Aspartate) Receptor

A
  • NMDA is an exogenous agent that activates these receptors. •Glutamate, aspartate, etc… all activate them in the body.
  • When activated, the channel allows influx of calcium. •Has multiple modulatory sites
  • GLYCINE binding site
  • Magnesium (Mg++) binding site

**PCP binding site •Horse tranquilizer
•Blocks channel

148
Q

AMPA Receptor

A
  • AMPA
  • Exogenous agent AMPA activated (really long chemical name, just know AMPA)
  • Glutamate/Aspartate are the endogenous ligands
  • Sodium influx when open
  • Benzodiazepines bind to a site on the extracellular face of the protein
  • Reduce the amount of sodium that enters.
149
Q

DOWNSIDE OF NO (nitric oxide)

A

•Vary unstable – half-life is about 5 seconds. •Leads to production of free radicals. •In high concentrations – toxic to neurons

150
Q

Brown-Séquard Syndrome

A

combination of sensory and motor deficits due to damage to ALS, PCML, & CST pathways.

• Knocks out half of the spinal cord
• Contralateral
o Loss of nociceptive, thermal (ALS; @ 2 segments below lesion)

• Ipsilateral
o Loss of discriminative tactile, vibratory, and
position sense, at/below the level
o Paralysis of the trunk and extremity(CST)
dependent of lesion level

151
Q

Syringomyelia

A

cystic cavitation of central region of SC (C3-T2)

Syrinx enlarges due to fluid accumulation and damages neural tissue.

• Initial damage to ALS fibers in AWC
• Usually progresses to anterior horn causing
motor deficits
• Distinct deficits in a cape like pattern
o Loss of pain and temperature bilaterally over the arms and shoulders
o Weakness, atrophy, and fasciculations of muscles of the hands

Neuroendocrine (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions