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171 Cards in this Set

  • Front
  • Back

Dermatome

An area of skin that is innervated by afferent axon fibres.

Slow Adapting Sensory Receptors

Aka tonic receptors. Detect strength of a stimulus and are important when maintaining information about a stimulus is valuable

Fast Adapting Sensory Receptors

Aka phasic receptors. Detect changes in stimuli and are useful when important to signal changes in stimuli or to stop paying attention to stimuli

First Order Neurone

Peripheral receptor --> spinal cord (synapse)
Cell body in sensory ganglion

Second Order Neurone

Spinal cord --> decussates --> ascends --> thalamus (synapse)
Cell body in spinal cord or brainstem

Third Order Neurone

Thalamus --> somatosensory cortex

Nociception

Sensory component of pain

First Pain

Feels sharp, fast transmission via A delta fibres

Second Pain

Dull/burning, slow transmission via C fibres

Hyperalgesia

Enhanced painful response to a normally painful stimulus

Allodynia

Painful response to a normally, non-painful stimulus due to a shifted pain threshold

Primary Hyperalgesia

Increased pain sensitivity in damaged tissue

Secondary Hyperalgesia

Increased pain sensitivity distant from the site of injury

Glaucoma

Increased pressure in the anterior compartment of the eye due to decreased reabsorption of aqueous humour

Optic Disc

Blind spot on the retina where the optic nerve leaves the eye

Macula

Central retina

Fovea

All photoreceptors here are cones (no rods), meaning low sensitivity but high visual acuity

Phase Locking

Responses can only occur with frequency equal to or higher than that at which a neurone can fire action potentials

Sclera

Outemost layer of the eye

Uveal Layer

Middle layer of the eye. Mostly choroid but most anteriorly is ciliary body.

Retina

Innermost layer of the eye. An outgrowing of the CNS

Myopia

Short sightedness. Eyeball is elongated. Correct with concave lens.

Hypermetropia

Long sightedness. Eyeball is shorter. Correct with a convex lens.

Glue Ear

Middle ear becomes filled with fluid

Papilloedema

Swelling of the optic disc due to raised intracranial pressure causing stasis of axoplasmic flow.

Reflex

Normally protective motor patterns generated in the spinal cord. closed loop with no input from higher centres.

Rhythmic Motor Patterns

Combination of reflex and voluntary motor patterns. e.g. chewing, walking, breathing.

Voluntary Motor Patterns

Purposeful, goal directed movements with command from higher centres.

Area 4

Cortical motor area that is responsible for distal muscle and fine motor control. It has the lowest stimulus threshold due to strong synaptic links.

Area 6/Premotor Area

Cortical motor areathat is involved in more complex movements. Proximal muscle control, balance, gait, preparation for movement, planning, initiation and bimanual coordination.

Comparator

Identify and correctdiscrepancies between descending motor signals (intended movement) and ascending afferent information (actual movement).

Timer

Sequence of motor activation to give smooth performance of movements followed by appropriate postural adjustment and maintenance.

Predictor

Enabling rapid execution of movements based on prior experience and expectation

Motor memory

Instigating learned motor sequences when appropriate

Posture Regulation

Indirect by adjusting major descending motor output

Hemiballismus

Caused by damage to the substantia nigra. Violent flailing limb movement on the contralateral side to the damage.

Tardive Dyskinesia

Caused by increased sensitivity of dopamine receptors due to long term use on antipsychotics. Uncontrolled movement of facial and trunk muscles.

Arousal

A state of wakefulness

Consciousness

Arousal + content. awareness of both self and external environment determined by a motor response to internal or external stimulus

Coma

Total absenceof awareness of both self and external environment

Oculovestibular Reflex

Cold water in one ear results in a slow deviation of gaze to the side of cooling then fast phase opposite

Oculocephalic Reflex

Move head - conscious eyes move with head, unconscious eyes stay in original position.

Physical Dependance

Anxiety, insomnia, cramps, tachycardia, piloerection, diarrhoea

Psychological Dependance

Compulsive behaviour, anxiety, depression

Epilepsy

A tendency toward recurrent seizures unprovoked by systemic or neurological traits

Epileptogenesis

Sequence of events that converts a normal neuronal network into a hyperexcitable network

Seizure

The clinical manifestation of an abnormal and excessive excitation of a population of cortical neurones. Abnormal, synchronous, paroxysmal neuronal discharge in the brain causing abnormal function

Status Epilepticus

An epileptic seizure that lasts for 30/10 mins or longer, or a series of seizures without regaining consciousness in between

Beta Waves

>14Hz active wakening, dreaming

Alpha Waves

8-13Hz quiet waking

Theta Waves

4-7Hz sleep

Delta Waves

<4Hz deep sleep, coma

Sleep Paralysis

During REM if dreaming of moving the motor cortex demands movement. The brainstem inhibits spinal motor neurones causing paralysis except for eyes and breathing.

Narcolepsy

Suddenly fall asleep

REM Sleep Behaviour Disorder

Loss of some sleep paralysis causing individuals to act out dreams

Ageing

The gradual changes in the structure and function that occur with time, that do not result from disease or gross accidents, and lead to the increased probability of death as the person grows older.

Bradykinesia

Slowness and impersistence of movement, less facial expressiveness, small writing, flexed trunk, Simian arm posture.

Aphonia

Low volume of speech or the absence of spoken language due to muscle weakness and vocal cord paralysis

Dysarthria/Anarthria

Failure of articulation. Causes: partial vocal cord paralysis, oropharyngeal problems, badly fitting dentures, cerebellar or brainstem pathology

Aphasia

Inability to transfer through into language due to poor comprehension, impaired expression or various combinations (Broca's, Wernicke's)

Emotion/Affect

Combination of psychological and physiological responses to a stimulus

Depression

Inability to experience pleasure or be happy, disorder of mood/affect

Anxiety Disorder

An inappropriate or excessive anticipatory manifestation of the fear response to a stressor

Schizophrenia

A severe psychiatric disorder characterised by disorder of though, perception and mood

Learning

Acquisition of knowledge

Memory

Retention of knowledge

Declarative Memory

Memory that you are consciously aware of, able to describe in words. This fades with time - not lost but becomes more difficult to retreive. May be semantic (facts) or episodic (with a time element).

Non-Declarative Memory

Memory of skills, habits and behaviours - procedural memory of motor tasks.

Retrograde Amnesia

Loss of events before the trauma

Ribot's Law

In the case of retrograde amnesia, more recent memories are more likely to be lost than remote ones.

Anterograde Amnesia

Inability to form new memories

Anaesthesia

The abolition of sensation

Triad of General Anaesthesia

Unconsciousness, analgesia, muscle relaxation

Lipid Theory

Lipid solubility is an important factor in general anaesthesia. Concentration in cell membrane of 0.05mM gives analgesia. Lipid volume expanded by 0.4%. High pressure reverses.

Protein Theory

Proteins are targets and lipid solubility is required for access to binding domains in hydrophobic pockets

Cut off Phenomenon

Increased chain length of general anaesthetics increases lipid solubility but does not increase anaesthetic potency and this stops at C13

Stereoselectivity

Identical lipid solubility but potentially different anaesthetic potencies

Minimum Alveolar Concentration

A measure of anaesthetic potency in man. The concentration of anaesthetic in the alveoli required to produce immobility in 50% of patients when exposed to a noxious stimulus.

Pain

An unpleasant sensory and emotional experience with actual or potential tissue damage

Features in the Midbrain

Superior colliculus, substantia nigra, red nucleua, oculomotor nucleus, inferior colliculus, trochlear nucleus, superior cerebellar peduncle, cerebral aqueduct runs through

Features in the Pons

Superior cerebellar peduncle, corticospinal/corticobulbar/pontocerebellar fibres, trigeminal nerve leaves, 4th ventricle runs through

Features in the Medulla

Inferior cerebellar peduncle, pyramids, NTS, dorsal motor nucleus of vagus, hypoglossal nucleus and nerve, inferior olivary nucleus, 4th ventrical rostrally, fasciculus cunteatus, fasciculis gracilis

On Ganglion/Bipolar Cells

Depolarised in light, hyperpolarised in dark

Off Ganglion/Bipolar Cells

Hyperpolarised in light, depolarised in dark

Direct Transmission Through Retina

Photoreceptor --> bipolar cell --> ganglion cell

Indirect Transmission Through Retina

Input from receptive field --> horizontal and amacrine cells --> bipolar and ganglion cells --> opposite electrical response to that in the centre --> contrast image borders

Ageusia

Loss of sense of taste

Middle Ear Attenuation Reflex

Contraction of tensor tympani and stapedius muscles in order to decrease movement of ossicles and therefore decrease middle ear conduction.

Characteristic Frequency

The frequency at which a neurone responds to the smallest sound intensity

Tonotopy

Special arrangement of structures that subserve various frequencies as in the auditory pathway


Lower frequency - anterior cochlear nucleus


Higher frequency - posterior cochlear nucleus

Phase Locking

Responses can only occur with frequency equal to or higher than than at which a neurone can fire action potentials

Closed Angle Glaucoma

When the iris adheres to the cornea blocking the reabsorption of aqueous humour.

Open Angle Glaucoma

When reabsoprtion of aqueous humour is reduced due to sclerosis of small veins/ This results in smaller increasing pressure of a longer period of time

Treatment of Glaucoma

Surgery to open the angle


Beta blockers to decrease the production of aqueous humour


PG analogues to increase blood drainage

Cortical Dysgenesis

Poor formation of the cortex

Lissencephaly

Smooth cortex, disorganised layers, fewer neurones resulting in significant functional impairment and decreased lifespan

Axon Guidance

Axons extend and grow towards correct targets

Fasciculation

Groups of axons grow together to form white matter tracts

Nystagmus

Jerking eye movements - normal when at the very periphery, pathological when

Hypokinetic Motor Dysfunction

e.g. Parkinsons

Hyperkinetic Motor Dysfunction

e.g. Huntingtons, Hemiballism, Tardive Dyskinesia

Huntingtons

Loss of striatal output neurones in the indirect basal ganglia pathway resulting in suppression of the substantia nigra so the direct pathway predominates. This means there is less output from the basal ganglia and therefore increased movement.

Huntingtons Inheritance

Autosomal dominant


CAG repeat


Shows anticipation

Parkinsons

Loss of dopamine in basal ganglia resulting in excessive inhibitions of the thalamocortical pathways and therefore less moevement.

Clouding of Consciousness

Lack of attention, slow thinking, confusion, memory loss, drowsiness

Delirium

Lack of attention, slow thinking, confusion, memory loss, drowsiness, disorientation, hallucination

Stupor

Sleep-like state, rousable with vigorous stimulation

Hypersomnia

Excessive drowsiness, intermittent waking

Decorticate

Abnormal flexion of arms and extension of legs. Indicative of hemispheric dysfunction

Decerebrate

Abnormal extension of arm and leg.


Indicative of upper brainstem dysfunction

Flaccidity in coma

Indicates pontine medullary damage

Signs of Cerebellar Dysfunction: DANISHP

D - dydiadochokinesia


A - ataxia


N - nystagmus


I - intention tremor


S - slurred speech


H - hypotonia


P - past pointing

Dydiadochokinesia

Inability to perform rapid alternating movements

Variability of Dependance

Drug - degree of reward


User - absorption/metabolism


Environmental - peer pressure

Tolerance Mechanisms

Innate - genetics


Metabolic


Behavioural


Pharmacodynamics

Behavioural Tolerance

Learn to behave normally even though under the influence

Pharmacodynamic Tolerance

Cell biology changes so that more receptors need to be activated for the same effect

Mechanism of Action of Opiates

Bind to GABAergic u opioid receptors in CNS --> dopamine release

Treatment for Opioid Overdose

Naloxone - blocks opioid receptors

Treatment for Opioid Dependance

Methadone - u receptor agonist with a longer half life, slower physical symptoms of withdrawal, don't get a good rush from heroin so less incentive


Psychotherapy

Caffeine Withdrawal Syndrome

Lethargy, irritability, headache

Mechanism of Action of Caffeine

PDE inhibitor --> increased cAMP


Adenosine receptor antagonist --> awake

Mechanism of Action of Cocaine

Inhibits catecholamine uptake (dopamine, noradrenaline) --> reward

Mechanism of Action of Amphetamines

Catecholamine release --> reward

Mechanism of Action of MDMA

5-HT release --> reward

Post Traumatic Stress Disorder

Triggered re-induction of a strongly emotional memory causes anxiety

Mechanism of Action of Benzodiazepines

Aloosterically binds to GABAa receptor in prefrontal cortex --> increases GABA affinity -->increases Cl- influx --> hyperpolarisation --> less active neurones

Anxiolytic

Reduces anxiety and aggression

Hypnotic

Sleep inducing

Benzodiazepine Withdrawal Symptoms

Increased anxiety, tremor, seizure, insomnia, depression

Mechanism of Action of Buspirone

5-HT partial agonist

Monoamine Theory of Depression

Depression is due to hypoactivity at monoaminergic (NAd and 5-HT) synapses in the brain.

Evidence for the Monoamine Theory of Depression

Antidepressants increase the levels of monoamines in the brain within minutes

Evidence Against the Monoamine Theory of Depression

Antidepressant take >1-3 weeks to work


Amphetamine releases monoamines, cocaine blocks monoamine reuptake but neither are antidepressants

Unwanted Effects of MAOIs

Cheese reaction due to unmetabolised tyramine in diet (cheese, red wine, yeast extracts, fermented soya bean)


Antimuscarinic effects


Alpha-1 antagonism

Mechanism of Action of Tricyclic Antidepressants

Inhibit uptake of 5-HT and NAd

Unwanted Effects of TCAs

Antimuscarinic effects


Sedative (histamine receptor 1 antagonism)

Stages of Anaesthesia

Analgesia


Delirium/Induction Phase


Surgical Anaesthesia


Medullary Paralysis

Induction Phase

Excitement, delirium, incoherent speech, loss of consciousness, unresponsive to non-painful stimuli, muscle rigidity, spasmodic movements, cardiac arrhythmias, vomiting, choking

Surgical Anaesthesia

Unresponsive to painful stimuli, breathing regular, abolition of reflexes, muscle relaxation, synchronised EEG

Medullary Paralysis

Pupillary dilation, respiration/circulation ceases, EEG wanes --> death

Divergent Connections

To generate an epileptic seizure, excitatory neurones must make divergent connections into a synaptic network

Effective Synapses

To generate an epileptic seizure, synapses need to be strong enough to drive a post synaptic effect

Minimum Aggregate

To generate an epileptic seizure, the population of neurones involved must be large enough so that they can connect to almost every other neurone in the population within a few synapses.

Focal/Partial Seizures

Originate in a specific part of the brain, localised to one hemisphere.


Last for 10 secs to 2-3 mins


Features dependent on location

Jacksonian March

Seizure starts in one are of the brain and progresses to other areas

Generalised Seizures

Seizures involving synchronicity in both hemispheres

Simple Partial Seizures

No altered consciousness

Complex Partial Seizures

Altered consciousness

Causes of Epilepsy in Infancy and Childhood

Birth injury


Inborn errors of metabolism


Congenital malformation

Causes of Epilepsy in Childhood and Adolescence

Idiopathic


Geneic syndromes


CNS infection

Causes of Epilepsy in Adolescence and Young Adults

Head trauma/Traumatic brain injury

Causes of Epilepsy in Older Adults

Stroke


Brain Tumour

Positive Symptoms of Schizophrenia

Delusions


Hallucinations


Disorganised speech


Grossly disorganised or catatonic behaviour


"inserted thoughts" - thought disorder

Negative Symptoms of Schizophrenia

Reduced expression of emotion


Social withdrawal


Cognitive impairment

Typical Neuroleptics

Phenothiazines (e.g. chlorpromazine, fluphenazine)


Butyrophenones (e.g. haloperidol, droperidol)


Thioxanthines (e.g. flupenthixol, clopenthixol)

Mechanism of Action of Typical Neuroleptics

Block dopamine receptors (D1 and D2)


-->antipsychotic effect


MAChR


H1


alpha NAdR


5-HT

Mechanism of Action of Atypical Neuroleptics

Dopamine receptor antagonists (sulpiride, amisulpiride)


Multiacting receptor targeted agents (clozapine, olanzapine)


Serotonin-dopamine antagonists (risperidone, zotepine, sertindole)

Dopaminergic Side Effects of Antipsychotics

Anti-emetic - reduces nausea dues to D2R and H1R block


Increased prolactin release (due to blocked dopamine) --> breast swelling, pain, lactation


Extrapyramidal motor symptoms (acute - dystonias, chronic - tardive dyskinesia)

Dystonia

Involuntary movements (face, tongue, neck), parkinsonian tremor.


Due to dopamine receptor blockade in striatum


Rapidly develops


Reversible

Non-Dopaminergic Side Effects of Antipsychotics

Antimuscarinic effects - dry mouth, constipation, visual disturbances


Postural hypotension due to adrenoceptor block


Sedation due to H1R block

Aetiology of Schizophrenia

Hereditary (50% chance in identical twins)


Environmental (cannabis)


? Slow viral infection, autoimmune, poor maternal nutrition, developmental abnormality


Genetic predisposition with environmental trigger


Dopamine hyperactivity

Evidence for the Dopamine Hypothesis of Schizophrenia

Amphetamine abuse


- releases dopamine


- toxic psychosis - paranoid delusions, hallucinations, compulsive behaviours


D2R agonists (apomorphine, bromocriptine)
--> positive symptoms


Too much L-DOPA
--> positive symptoms
- dose reduced --> disappear

Grandmother Cell Hypothesis

Every memory is assigned to a single neurone

MND/ALS

Limb/bulbar paralysis on onset but sensation is spared


Damage to ventral horn cells

Broca's/Expressive Aphasia

Non-fluent speech


Normal comprehension


Poor naming and repetition

Broca's Area

Inferior frontal lobe, adjacent to motor cortex for cranial nerves to mouth and larynx

Literal Paraphasic Speech

Incorrect sound e.g. 'ren' for 'pen'

Verbal Paraphasic Speech

Incorrect word e.g. 'fork' for 'pen'

Wernicke's Aphasia

Fluent speech empty of meaning


Comprehension impaired


Often unaware/unconcerned

Anomia

Inability to produce a specific name