NE Exam 2 Clinical Flashcards

Question

TRPM8

Answer 1

``` Cooling agents (ex. camphor or menthol - used for their analgesic properties) Ex. topicals: Vicks Vaporub, Biofreeze, Oral-B oragel ```

Answer 2

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

Answer 3

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

Answer 4

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.

Answer 5

``` Cooling agents (ex. camphor or menthol - used for their analgesic properties) Ex. topicals: Vicks Vaporub, Biofreeze, Oral-B orajel ```

Answer 6

Occlusion of AICA Ataxia, unsteady gait, fall toward side of lesion

Answer 7

Vertigo, nausea, nystagmus, deafness, tinnitus, | vomiting (at caudal levels)

Answer 8

Ipsilateral paralysis of facial muscles

Answer 9

Ipsilateral paralysis of masticatory muscles

Answer 10

Ipsilateral Horner syndrome

Answer 11

Ipsilateral loss of pain and thermal sense from | face

Answer 12

Contralateral loss of pain and thermal sense from | UE, trunk, and LE

Answer 13

Paralysis | of conjugate horizontal gaze

Answer 14

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)

Answer 15

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

Answer 16

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

Answer 17

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

Answer 18

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)

Answer 19

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

Answer 20

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.

Answer 21

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

Answer 22

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

Answer 23

The thalamogeniculate branches of the posterior cerebral artery. Complete loss of discriminative touch, pressure sensation, and proprioception to the contralateral body.

Answer 24

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

Answer 25

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

Answer 26

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

Answer 27

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

Answer 28

VMAT2. Reserpine inhibits this process. Leads to synaptic failure

Answer 29

knock-out mice are obese and seizure prone

Answer 30

located in area postrema --> induces vomiting

Answer 31

anti-depressant effect

Answer 32

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.

Answer 33

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

Answer 34

Broad-based, staggering gait note: think of ataxia as symptoms you'd have while drunk

Answer 35

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

Answer 36

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

Answer 37

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.

Answer 38

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.

Answer 39

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.

Answer 40

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

Answer 41

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.

Answer 42

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

Answer 43

Lesions of the vestibulocerebellum may result in nystagmus. | Irregular movements of the eye

Answer 44

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.

Answer 45

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.)

Answer 46

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.

Answer 47

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.

Answer 48

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.

Answer 49

Unilateral lesions of the subthalamus result in hemiballismus

Answer 50

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.

Answer 51

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

Answer 52

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.

Answer 53

Sign & Symptoms: Slow, involuntary, writhing movements of the limbs & face. Due to: Degeneration of the striatum.

Answer 54

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.

Answer 55

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.

Answer 56

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

Answer 57

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

Answer 58

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.

Answer 59

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)

Answer 60

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.

Answer 61

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.

Answer 62

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.

Answer 63

indicates involvement of corticospinal tract.

Answer 64

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.

Answer 65

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)

Answer 66

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.

Answer 67

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

Answer 68

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

Answer 69

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

Answer 70

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

Answer 71

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

Answer 72

have minimal clinical effect

Answer 73

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)

Answer 74

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

Answer 75

result in paralysis or paresis of the distal limb muscles below the level of the lesion. (ipsilateral or contralateral depends on location of lesion)

Answer 76

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

Answer 77

● 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.

Answer 78

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

Answer 79

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.

Answer 80

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.

Answer 81

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.

Answer 82

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

Answer 83

``` 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

Answer 84

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

Answer 85

``` 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 ```

Answer 86

``` 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.

Answer 87

• 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

Answer 88

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

Answer 89

o Ipsilateral flaccid paralysis of upper and lower face

Answer 90

• 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

Answer 91

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.

Answer 92

* 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.

Answer 93

* 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.

Answer 94

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

Answer 95

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.

Answer 96

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.

Answer 97

● (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

Answer 98

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.

Answer 99

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

Answer 100

: 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

Answer 101

: 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

Answer 102

: 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.

Answer 103

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

Answer 104

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.

Answer 105

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).

Answer 106

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.

Answer 107

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.

Answer 108

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.).

Answer 109

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

Answer 110

•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

Answer 111

* 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

Answer 112

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.

Answer 113

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

Answer 114

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)

Answer 115

* The endorphins(endogenous morphines– we knew about morphine first). * The enkephalins * The dynorphins * Nociceptin

Answer 116

* 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.

Answer 117

* 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.

Answer 118

Exogenous chemicals (THC –Δ9-Tetrahydrocannabinol). Endogenous cannabinoids are: Anandamide 2-Arachidonylglycerol (2AG)

Answer 119

* 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

Answer 120

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

Answer 121

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.

Answer 122

* 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.

Answer 123

* 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

Answer 124

* 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.

Answer 125

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

Answer 126

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

Answer 127

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

NE Exam 2 Clinical Flashcards

(151 cards)