SHS 280 Neuroscience Exam 1

Motor Cortex

The motor cortex is what controls volitional movement (i.e., movement you choose to make).

The motor cortex can be divided into the premotor cortex and the primary motor cortex.

Reflexes

Lrgely involuntary movements, typically controlled primarily by the spinal cord, such as when you pull your hand back after touching something sharp.

Premotor Cortex

involved in planning actions. It allows you to plan out which muscles you are going to move and in what way you are going to move them before you actually start moving your muscles. The premotor cortex primarily sends connections to the primary motor cortex.

Primary Motor Cortex

plays a role in executing motion. Individual neurons in the primary motor cortex affect individual muscle groups. The primary motor cortex also receives input from the somatosensory cortex, particularly proprioception, which tells you where your body is in space.

Proprioception

tells you where your body is in space.

Homunculus

mini representation of the body that is set up within the motor cortex, referred to as a homunculus. Critically, the size of different body parts in the homunculus relate to the number of neurons that are involved in the control of that body part, which in turn reflects the precision of motor control for that body part.

Plasticity

ability to change the representation of parts of the body within the primary motor cortex. Not static throughout your life. Key to allowing you to gain skills and learn new information throughout your life.

Basal Ganglia

one of the structures that is involved in modifying the motor plan designed by the premotor cortex. The basal ganglia forms loops, taking the motor plan from the motor cortex, modifying it, and sending it back up to the motor cortex. The basal ganglia makes two types of changes: it increases the likelihood of producing the desired movements and it decreases the likelihood of producing the undesired movements.

hypokinetic disorder

Produce too little movement. those that occur with Parkinson’s disease, involve reduced movements, including difficulties initiating movements. One of the hallmarks of hypokinetic disorders is a slow, shuffling walk

hyperkinetic disorder

Produce too much movement. such a Huntington’s disease, involve additional movements on top of the desired movements, often resulting in jerky movements

excitatory connections

having a value of +1

inhibitory connections

having a value of -1

determine if the net effect of a pathway will be more motion (+1) or less motion (-1)

multiply the values for each of the connections together.

Direct pathway

net effect of the direct pathway is excitatory – it increases the likelihood of creating motion. Even # of inhibatory

Indirect pathway

Odd # of inhibitory. net effect of the indirect pathway is inhibitory.

substantia nigra

major source of dopaminergic neurons (i.e. neurons that produce dopamine). This is a critical input into the motor system that helps you produce movement. If these neurons die, such as occurs with Parkinson’s, you will have difficulties initiating movements.

Normally, it increases the gain in the direct pathway, resulting in more excitation and thus more movement. It also normally decreases the gain in the indirect pathway, resulting in less inhibition and thus also more movement

Nucleus Accumbens

Sometimes referred to as the devil’s playground, this is the central structure for reward. It also plays a key role in addiction. Almost anything that is pleasurable or addictive activates the nucleus accumbens. The nucleus accumbens relies on a particular neurotransmitter, dopamine, that plays important roles throughout the basal ganglia and other parts of the brain.

Cerebellum

CN I

Olfactory related to the sense of smell

CN I Olfactory

Receptors are replaced every 30 - 60 days

Degeneration of olfactory cells and fibers can occur with age or damage

Can be unilateral or bilateral (1 or both nostrils)

Anosmia (damage to olfactory nerve)

Complete loss or inability to detect odors. Can be temporary (from a bad cold) or permanent (head trauma)

Hyposmia (damage to olfactory nerve)

Reduced or decreased ability to smell & detect odors

Hyperosmia (damage to olfactory nerve)

Abnormally heightened & oversensitive sense of small triggered by hormones (pregnancy), migraines

CN II

Optic - •Carries visual information from the eyes to the brain

Does not move the eyes

•Goes from the retina through the lateral geniculate body to the visual cortex

•Result of damage highly dependent on the location of the lesion

CN III

Oculomotor - controls all the rest of the eye muscles. Looking up, down, inward, lifting your eyelid, focusing your lens for near/far objects

CN IV

Trochlear - superior oblique muscles. Uses tiny tissue pulley to rotate your eye down & inward (looking down at book or phone)

CN VI

Abducens - lateral rectus muscle. Think of abduction (to kidnap/take away) muscle pulls eyes outward away from midline (looking to the side)

CN II, III, IV, VI

Reading, lipreading, sign language

•Allows you to move your eyes, focus on nearby/far objects, and see what you are looking at

Controlling eye movement

•The brainstem gaze centers coordinates the activity across the oculomotor, trochlear, and abducens nerve

Speaking & Signing

CN V, VII, IX, X, XI, XII

CN V

Trigeminal - Move your jaw

CN VII (7)

Facial - Move your lips

•Controls muscles involved in

–Facial expression/lip movement

CN IX (9)

Glossopharyngeal – Move your pharynx

Pharynx controls upper throat

CN X (10)

Vagus – Control your larynx

Larynx controls lower voice box

•Provides sensory information from the larynx

–Important for modulating your voice

CN XI (11)

Spinal accessory - Shrugging

Head rotation

CN XII (12)

Hypoglossal – Move your tongue

•Has unilateral innervation

Damage to Trigeminal nerve (CN V)

Bilateral jaw

Paralysis

How would bilateral jaw paralysis affect speech?

Causes the lower jaw to hang wide open due to gravity, impossible to close the mouth

Distorts bilabial and fricative and other sounds

Damage to CN XI (11)

•Damage results in impaired ability to

–Rotate the head laterally

–Raise the shoulders

Damage to CN XII (12)

•Damage can result in

–Ipsilateral paralysis of the tongue causing it to be wrinkled and atrophy

–Tongue deviation to side of lesion

–Chewing difficulty

•Bilateral damage can result in profound difficulty swallowing, eating, and speaking

CN VIII (8)

(auditory and vestibular nerve) – hear what you and others say

CN VII (7) Sound part

(facial nerve) – stapedial response that quiets loud sounds, including those self-made

Auditory System Disorders

•Can involve periphery system or central system

•Affects on periphery system are much more common

•Typically disorders affecting the central auditory system also affect other systems

Conductive Hearing Loss reflects a problem before the

Inner ear

•Something blocking the ear canal

•Damage to the middle ear bones

Conductive Hearing Loss results in sound being

Softer

•Outer (and inner) hair cells are still intact

•If you make things louder or directly vibrate bone, sounds will not be muddy

Many medicines can damage

Hair Cells

Ototoxicity

Ear poisoning - a pharmacological adverse reaction that occurs when exposure to certain medications occurs chemical substances damages the structures of the inner ear or vestibulocochlear nerve.

Ototoxicity: Many medicines can damage

Hair Cells (in the inner ear)

Ototoxicity: The effects can be

Temporary or Permanent

Ototoxic effects often only occur after taking

Abnormally large quantities of the medication

Common examples of ototoxic medications

•Gentamicin (antibiotic)

•Cisplatin (for cancer)

•Vicoden (for pain)

•NSAIDS (for pain)

Aspirin

Advil

Aleve

Noise exposure drives increased

metabolic activity

Noise Exposure Causes the buildup of

Reactive oxygen species causing cell death

Noise exposure: Initial signs often involve a

“noise notch” (V-shaped drop in hearing sensitivity on an audiogram occurs btw 3-6 kHz – indicator of early-stage noise-hearing loss) in the audiogram at around 3 kHz

The most common genetic mutations resulting in congenital hearing loss affect

Connexin 26

Connexin 26 is a

Critical protein for forming gap junctions that are responsible for maintaining the K+ concentration in the endolymph

Genetic mutations: DFNB12 (x3)

•DFNB12 is another mutation associated with hearing loss

•This causes a progressive loss of tip links in animals

•In humans it results in congenital deafness

Ménière's disease

Appears to be caused by excess fluid in the inner ear

Ménière's disease Symptoms are often fluctuating and include:

Vertigo (Dizziness/spinning)

Hearing loss

Sense of fullness in the ear (Pressure like being underwater)

Tinnitus (Ringing in the ear)

Ménière's disease Treatments are still being researched

Labryinthectomy

Trans-tympanic steroids

Pressure pulses delivered to the ear

Low salt diet

Medications

Auditory Neuropathy reflects problems with the

transmission for signals from the cochlea to the brain

Auditory neuropathy Often seems to be related to a decrease in the

synchrony of firing in the auditory nerve

Auditory neuropathy Generally diagnosed by the presence of

Normal otoacoustic emissions alongside any missing or abnormal auditory brainstem response

Patients with auditory neuropathy often have

normal pure tone thresholds but exceeding difficulty in noisy environments

Patients with auditory neuropathy tend to also have difficulties with

tasks such as gap detection

Generally Auditory Neuropathy deficits are consistent overtime, but there are cases where symptoms only occur while the patient has a

Fever

There has been some success treating auditory neuropathy patients with

Cochlear implants

Acoustic Neuroma (x4)

•Tumors can develop on CN VIII (leading from your inner ear to your brain)

•These are generally slow-growing and benign (non-cancerous)

•If they grow sufficiently large they may be removed surgically, generally cutting CN VIII

•Acoustic neuromas are a major reason that patients presenting with asymmetric losses may be referred for an MRI

Wernicke’s Aphasia

•Wernicke’s Aphasia is primarily a comprehension problem

•These patients often do not seem frustrated

Wernicke’s Aphasia they have

•fluent but generally meaningless speech

•Their speech contains many neologisms

•They have impaired repetition

Tumors can occur in

many places along the auditory pathway

Tumors in the auditory pathway are often

Benign (non-cancerous)

Tumors in the auditory pathway can push against structures as they grow and cause a

Wide variety of problems

Neurofibromatosis Type 2 (x4)

•Genetic disorder

•Results in a proliferation (rapid/massive increase in number) of tumors in the nervous system

•The tumors generally grow slowly

•Almost always involves tumors on CN VIII

NF2 auditory symptoms

•Hearing loss

•Can be severe enough that it requires a cochlear or brainstem implant

•Tinnitus (Ringing in the ears)

NF2 non-auditory (x4)

•Balance problems

•Numbness or weakness of part of the body (tumors near spinal cord)

•Headaches and seizures (tumors in the meningioma pressing on the brain)

•Cataracts (When the naturally clear lens in your eye becomes cloudy, acting like a foggy or frosted window that blurs your vision)

NF2 treatment

•Active area of research

•Currently more about management than treatment

•Annual MRIs

•Annual vision checks

•Annual hearing tests

Even though the tumors are generally benign, as they grow they can

press against the nervous system

This can eventually be fatal and large tumors need to be removed

Presbycusis

•Age-related hearing loss

•Has an environmental component

•Noise-induced hearing loss involves a trade-off between time and sound level

•Has a genetic component

•Probability of having presbycusis greater if a near blood relative also has it

Presbycusis potential genetic components

•Increased susceptibility to hearing loss

•Genetic evidence from patients with presbycusis suggests affected regions similar to those for congenital hearing loss

Presbycusis - Increased protection from hearing loss

Some elderly individuals seem to have typical noise exposure but never develop a hearing loss

Presbycusis Symptoms:

•Symptoms include

•Lack of clarity of speech

•Inaudibility of sounds

•Difficulty in noisy environments (often not explained by audibility issues)

•Hyperacusis (normal sounds feel painfully loud – think of someone hungover)

•Tinnitus

•Loss of temporal acuity (Brain’s ability to process time-related details in sound – tiny gaps btw syllables or rapid changes in a sentence)

•Decreased contralateral suppression of OAE (Brain loses its ability to suppress or filter out background static)

Presbycusis effects

Peripheral effects: Audibility effects

Central effects: Listening in noise difficulties not accounted for by audibility issues

Multiple sclerosis (x3)

•This is a demyelinating disease

•It causes a wide variety of symptoms

It does also rarely result in hearing problems

Multiple sclerosis - Some hearing problems that occur in a subpopulation of patients

•Hearing loss

•Difficulty in noisy environments

•Lateralization difficulty

•Can reflect both interaural time and level differences

Stroke

•Strokes occasionally affect auditory functions

•What functions are affected depends on the location of the stroke