Saturday 26 October 2013

Neurotransmission

Action potential is the maximum positive charge generated within the axon as a result of a nerve impulse.

Synapses are specialised junctions where impulses pass from one neuron to the next.
  • A sensory neurone carries a nerve impulse from a receptor into the central nervous system.
  • A relay neurone carries a nerve impulse from the central nervous system to a motor neurone. 
  • A motor neurone carries a nerve impulse from the central nervous system to a skeletal muscle. 

There are two main types of cells in the nervous system:
1. Neurones, that are adapted to carry nerve impulses
2. Neuroglia, that provides structural and metabolic support to the neurones.

The basic structure of the neurone is:
1. A cell body containing a nucleus surrounded by a granular cytoplasm (perikaryon). The granules in the cytoplasm are referred to as Nissl substance and consist of dense clusters of rough endoplasmic reticulum.
2. An axon which conducts impulses away from the cell body to other neurones or to effectors.
3. One or more dendrites that are highly branched processes which carry impulses from specialised receptors or from adjacent neurones.

There are three types of neurones:

Type
Structure
Function

Multipolar neurones
Most common type. Have many dendrites.
They act as motor neurones.
Bipolar
neurones
Uncommon. Have one dendrite.
They act as receptors for sight, smell and balance

Pseudo-unipolar neurones
Have one dendrite
Act as sensory neurones.

  • Axons are surrounded by Schwann cells, which is called a myelin sheath.
  • Myelinated neurones are mostly found in sensory and motor neurones.
  • Unmyelinated are found in relay neurons and the autonomic nervous system.
  • Between the Schwann cells there are small gaps where the axon is not covered by myelin, known as nodes of Ranvier.
  • The conduction velocity of the nerve impulses is proportional to the diameter of the axon.
  • The conduction velocity of myelinated neurons is faster than that of unmyelinated neurons of the same diameter.
  • When a neurone is not conducting an impulse it is in resting state.

In resting state:
1. Large negatively charged organic ions are mainly on the inside the axon. This is because the membrane is impermeable to them. They cause the overall negative charge inside the axon.
2. Potassium ions are in greater concentration inside the axon. This is because there protein channels that allow K+ to pass through. They do not diffuse out down their concentration gradient because they are attracted by the overall negative charge inside.
3. Sodium ions are in greater concentration outside. This is because the permeability of the axon membrane to Na+ is low and also because they are expelled by ion pumps.
4. Chloride ion concentration is greater outside. Their concentration gradient is inward but they are repelled by the overall negative charge.

When an impulse is generated:
1. Sodium channels open and Na+ enter faster than they are expelled.
2. The overall charge inside the axon becomes positive. This is known as the action potential.
3. The permeability of the membrane to Na+ decreases and the permeability to K+ increases.
4. K+ flow out. Overall charge inside becomes negative.
5. Potassium ions continue to leave and the overall charge inside becomes slightly more negative than the when in resting potential. This is called hyperpolarisation.
6. Resting potential is restored as K+ and Na+ return to their resting concentration.

Saltatory conduction is when the action potential jumps from one node of Ranvier to the next and takes place in myelinated axons, greatly increasing the conduction velocity.

At a synapse an impulse travels from one neurone to the next.
There are two main types of synapse:
1. Electrical. This occurs when the two neurons are very close together.
2. Chemical. This is the most common.

In chemical synaptic transmission:

1. An action potential reaches the synaptic knob of the presynaptic neurone and calcium channels open. Calcium ions diffuse into the knob.
2. This increase in calcium ions stimulates the movement of vesicles containing a transmitter substance towards the presynaptic membrane.
3. The vesicles fuse with the membrane and release their substance by exocytosis into the synaptic cleft.
4. The transmitter substance diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane. This causes ion channels to open.
5. The movement of Cl, Na+, K+ in or out of the postsynaptic neurone generates a postsynaptic potential.
6. Depending on which ion moves in or out the postsynaptic membrane is either depolarised or hyperpolarised.
7. Depolarisation results in the development of an excitatory postsynaptic potential and hyperpolarisation results in an inhibitory postsynaptic potential.
8. The transmitter substance is quickly removed by enzyme action and diffusion.

There are four main groups of transmitter substances:

Transmitter substance
Function
Acetylcholine
Found at neuromuscular junctions and many parts of the brain
Amines e.g. noradrenaline.
In the sympathetic nervous system and some parts of the central nervous system
Amino acids e.g. glycine
Inhibitory substance in nerve pathways in the spinal cord.
Neuropeptides e.g. endorphins
Regions of the brain. Block pain.

Legionella Pneumonia

Caused by an aerobic bacteria belonging to the genus Legionella, which contains 20-30 species. Most commonly cause by Legionella pneumophilia, a gram negative bacteria. The bacteria can be found in any freshwater environment but in low numbers due to the low temperature. It is when the water is taken into artificial water systems and the temperature arises to around 20-45 degrees with impurities such as rust, limescale or algae that they start to multiply. 

Vulnerable water systems include:
  • Cooling towers
  • Air conditioning systems
  • Water systems for large buildings, such as hospitals, hotels or sports complexes

Symptoms
  • Flu like symptoms including mild headaches, fever, muscle pain and chills.
  • As the disease progresses to the lungs, a persistant cough appears with chest pains and shortness of breath.
  • Cough progresses from dry to mucus filled, possibly with blood
  • Approximately 30% of people also encounter D&V
  • Around 50% show signs of mental confusion

Risk Factors
  • Aged over 50 years
  • Smoking
  • Kidney Ulcer
  • Diabetes
  • COPD

Patients commonly end up on ICU, sometimes with a tracheostomy and the use of the Bird (IPPB) with vibs.

Friday 25 October 2013

Frozen Shoulder

Frozen Shoulder has no specific definition or cause. It can be primary (idiopathic) or secondary (T2DM, CV disease, hemiparesis, trauma or TB). It is also known as adhesive capsulitis, painful stiff shoulder, retractile capsulitis and monoarticular arthritis.

Symptoms
  • Pain felt near deltoid insertion
  • Inability to sleep on affected side
  • Painful and incomplete elevation and ER
  • No primary diagnostic test; AROM=PROM
  • Mistakable for bicipital tendonitis or impingement
    • Standard tests (e.g. Neers) positive during the painful phase as they stretch the joint capsule
  • ER most restricted, abduction, less, IR less still (Cyriax, 1982) although arthritis and fractures could cause a similar capsular pattern
  • Negative x-rays

Progression
  • Stage One - 'Freezing Stage'
    • Progressive stiffening
    • Loss of ROM
    • Increasing pain on mvt
    • 2-9 months
  • Stage Two - 'Frozen Stage'
    • Gradual decrease in pain, stiffness remains
    • Considerable loss of ROM
    • 4-12 months
  • Stage Three - 'Thawing Stage'
    • Improvement in ROM
    • 12-42 months

Treatment
  • Conservative Treatment
    • Medication
      • NSAIDS, opiods
    • Physio
      • Advice and education
      • Superficial heat or cold therapy
      • Electrotherapy
      • Exercise and mobilisation
  • Minimally Invasive Treatment
    • Injections
      • Hydrodilation
      • Corticosteroids
      • Sodium hyaluronate
    • Acupuncture
  • Invasive Treatment
    • Arthroscopic capsular release
    • Manipulation under anaesthetic

Physiotherapy Treatment - Stage III
  • Home Exercise Programme
    • ROM and strengthening
    • Progress from static to dynamic strengthening
    • Shoulde retraction and rolls
    • Pendular mvts in forward leaning
  • Mobilisation
    • End range and mobilisations with movement more effective than mid-range mobilisation (Yang et al, 2007)
  • Shoulder classes
    • Long-term
  • Education
    • Up to 17% of patients experience frozen shoulder in their other arm within 5 years

Duchenne Muscular Dystrophy

•  Most common muscular dystrophy
•  Progresses more rapidly than other dystrophies
•  20-30 of 100,000 males
•  X-linked recessive
•  Absence of large protein: dystrophin
•  Results in abnormal muscle degeneration with fat and connective tissue regeneration in its place
•  Pseudohypertrophy
•  Results in muscle weakness associated with wasting



Cerebellum

  • Primary function is to evaluate how well movements initiated by motor areas are actually being carried out eg coordination of movement
  • Cognition (acquisition of knowledge) eg learning from mistakes and feedback loop through thalamus
  • Regulates balance and posture
  • Found in the posterior fossa, inferior to the occipital lobe.

Three Areas:

Vestibulocerebellum
- Found on the inferior surface in the Flocculonodular (flok-u-lo-NOD-u-lar) lobe
- Receives vestibular and visual input
- Contributes to equilibrium and balance
- A lesion in this area results in disturbances in posture and gait

Spinocerebellum
- Found in the centre in the vermis
- Receives proprioceptive input

Cerebrocerebellum
- Found in the lateral hemispheres (anterior and posterior lobes)
- Governs subconscious aspects of skeletal muscle movements, ensuring a smooth orderly sequence of muscle contraction

Input and output is via the three pairs of large tracts known as the superior, middle and inferior peduncles.Dysfunction of the cerebellum will result in the inability to perform smooth directed movements, eg ataxia, kinetic tremor dysmetria (inaccuracy)

Thursday 24 October 2013

Dual Tasks

Dual task performance can be defined as an individual’s capability to complete two tasks concurrently (Pashler, 1994; O’Shea, Morris & Iansek, 2002; Yang, Wang, Chen & Kao, 2007; Kizony et al, 2010). The ability to dual task affects activities of daily living on a vast scale (O’Shea, Morris & Iansek, 2002; Sethi & Raja, 2012), with reduced dual task performance defined as a dual task cost (McCulloch, 2007). Dual task costs (DTC) have greater functional decrement in persons with neurological impairment (Kizony et al, 2010), which may result from pathology, such as Multiple Sclerosis (MS) (Sosnoff et al, 2013) and Parkinson’s Disease (PD) (O’Shea, Morris & Iansek, 2002; Mak, Yu & Hui-Chan, 2013), or natural aging processes (Beauchet et al, 2009; Yogev-Seligmann, Giladi, Brozgol & Hausdorff, 2010). However, the application of dual task theories is relevant to the wider patient population, with few studies researching the effect of dual task costs on a young, healthy population. Therefore, further research in this area may facilitate development of dual task strategies applicable to a wider spectrum of clinical specialities.  

Previous research has looked at the benefits of using dual task strategies as part of assessment, for example post-stroke (Yang, Wang, Chen & Kao, 2007) and to predict risk of falls (Beauchet et al, 2009). Additionally, dual tasks can be used as part of rehabilitation to improve safety in functional performance (Albinet, Bernard & Palut, 2006), for example by reducing dual task costs in persons with dementia (Schwenk, Zieschang, Oster & Hauer, 2010), improving balance in persons with a history of falls (Silsupadol, Siu, Shumway-Cook & Woollacott, 2006) and improving gait in older adults for safer road crossing (Silsupadol et al, 2009) and poststroke (Salbach et al, 2005; Yang, Wang, Chen & Kao, 2007). Furthermore, the use of traffic lights as an audio-visual cue can be utilised to enhance dual task walking performance in persons with PD (Mak, Yu & Hui-Chan, 2013). The frontal lobes are the areas of the brain most affected by the natural aging process, thereby implicating co-ordination and management functions (Kramer & Larish, 1995). This may partially explain why dual task decrement is reduced in a younger population compared to in an older population.

Dual task theories can be used to understand how the interaction between cognitive, perceptual, mechanical, and neurological components of dual task performance results in a dual task cost (Huang & Mercer, 2001). The bottleneck theory suggests that when two tasks are performed simultaneously, they require the use of the same neural machinery at the same point in time. The critical operations are carried out sequentially (Pashler, 1994), with one task delayed until the other task has been processed. For example, the bottleneck theory can be used to explain why some older adults stop walking in order to talk (Beauchet et al, 2009). The capacity-sharing model suggests that two tasks can be processed in parallel by dividing capacity between two or more resource pools. For example, an individual can walk and talk simultaneously but the speed or accuracy of one or both tasks will decrease. According to Pashler (1994) the crosstalk model assumes that similar tasks are easier to perform concurrently as use of the same pathway utilises less attentional resources and therefore increases the efficiency of processing. Navon & Miller (1987) state that crosstalk refers to the features or stimuli of two tasks overlapping. All three theories suggest that when more than one task is performed at any given instant, there is reduced capacity for individual tasks, resulting in a decline in performance in one or both tasks.

Dual tasks strategies are commonly used in falls assessment and rehabilitation as a progressive tool that facilitates functional training. It is additionally used in vestibular rehabilitation to train the components of balance to compensate for vestibular dysfunction. This can be transferred to neurological rehabilitation or musculoskeletal function to deal with reduced vision, central inputs or proprioception (for example with an ACL injury).

Subjective Assessment

History of Presenting Condition
  • How long the symptoms have been present
  • Slow or sudden onset
  • Known or unknown cause
  • Progression of symptoms
    • How are they today?
    • Pain scale?
  • Are they seeking treatment elsewhere?
  • Relationship of symptoms
  • Previous injuries
    • How many? Where? Cause? Duration? Recovery? Episode of stiffness?
  • Last hospital admission

Social History
  • In relevance to patient's onset, progression and recovery
  • Patient's perspective and experience
  • Patient's expectations
  • Age
  • Employment
  • Home situation
  • Social and work environment

Yellow Flags
  • Belief that pain is harmful or potentially disabling
  • Fear avoidance and reduced activity levels
  • Low mood and removal from social situations
  • Expectation that passive, rather than active, treatment will help

Symptoms

Area of current symptoms
  • Use of body chart - tick to indicate clear areas
  • If you had to identify your pain to one spot, could you point at it?

Pain
  • Quality
    • Bone = deep, dull nag
    • Muscle = dull ache
    • Nerve root = sharp and shooting
    • Nerve = sharp, bright and lightning like
    • Sympathetic nerve = burning and stinging
    • Vascular = throbbing, diffuse
  • Intensity
    • VAS
  • Timing
    • Pain on waking = inflammatory
    • Pain on rising = mechanical
  • SIN
    • Severity
      • The degree to which symptoms restrict movement and function
    • Irritability
      • The degree to which symptoms increase and reduce with provocation
      • When pain is aggravated, how long does it take to reduce?
    • Nature
      • Night/evening/morning symptoms
  • Depth of pain
  • Constant or intermittent
  • More than one area
    • Linked?
    • Same source?

Abnormal Sensation
  • Paraesthesia = abnormal sensation
  • Allodynia = pain provoked by stimuli that are normally innocuous
  • Analgesia = absence of appreciation to pain
  • Hyperaesthesia = heightened perception to touch

Tuesday 22 October 2013

Basal Ganglia

Deep within the cerebral hemispheres are five nuclei (masses of grey matter) collectively known as the basal ganglia. They are:

  • Globus pallidus and putamen (otherwise known as the lentiform nucleus).
  • Caudate nucleus (the putamen and caudate nucleus are collectively known as the striatum)
  • Substantia nigra (although located in the midbrain technically)
  • Subthalmic nuclei (although located in the midbrain technically)
  • Receives input from the cerebral cortex and provides output back to motor areas via the thalamus
  • Major function is to help initiate and terminate movements of the body
  • Also suppresses unwanted movements and regulates muscle tone.

Role of the Basal Ganglia in Motor Control
In a resting person the internal segment of the globus pallidus (GPi) and the pars reticulate of the substantia nigra (in the midbrain) sends spontaneous inhibitory signals to the thalamus, through the inhibitory neurotransmitter GABA. Inhibition of the excitatory neurones in the thalamus leads to a reduction of activity in the motor cortex’s and therefore a lack of muscular activity.

When the pre frontal region of the cerebral cortex (decision making and planning) initiates movement it sends signals to the motor cortex’s. These then send signals through the basal ganglia in order to decide which muscles will participate in the movement.
Direct loop ALLOWS MOVEMENT
  • The motor cortex’s send signals to inhibitory cells of the striatum (caudate and putamen)
  • They then send inhibitory signals to the internal segment of the globus pallidus (GPi) and the substantia nigra (with the inhibitory neurotransmitter GABA)
  • These inhibitory signals then stop the original spontaneous inhibitory signals (that usually happen in a resting person) meaning that the thalamus is now free to excite the motor cortex’s
  • This accelerates motor cortex activity and will eventually result in muscle contractions
  • Therefore two minus make a plus!!

Indirect loop INHIBITS UNWANTED MOVEMENT
  • Operates in conjunction with the direct loop to help prevent unwanted muscle contractions from competing with voluntary movements.
  • At the same time that signals are being sent through the direct loop, the motor cortex’s send signals to inhibitory cells of the indirect loop in the striatum (caudate and putamen)
  • These cells then send inhibitory signals to the external segment of the globus pallidus (GPe) reducing activity in that area.
  • The GPe normally send inhibitory signals to the Subthalmic nucleus
  • When the indirect loop is activated these inhibitory signals are reduced which leaves the Subthalmic nucleus free to excite the GPi and the substantia nigra
  • Which in turn are then free to send more inhibitory signals to the thalamus, which prevents the development of activity in the motor cortex
  • This loop prevents the activation of motor cortical areas that would compete with the voluntary movement
  • Therefore preventing unwanted muscle contractions (BOOM!!!)

Parkinson’sneurons in the substantia nigra release dopamine. The loss of these neurones and therefore the loss of dopamine results in overactive inhibition of the thalamus, causing bradykinesia (because the substantia nigra sends to many spontaneous signals to the thalamus which reduce muscular activity). Dopamine is also a modulatory neurotransmitter and the loss of it results in a change in tone, resulting in rigidity.

Huntington’sinhibitory signals (GABA) from the striatum to the GPe (indirect) and the GPi and substantia nigra (direct) are damaged. Damage to the indirect loop leads to chorea (random purposeless movements) and damage to the direct loop results in increased inhibition of the thalamus which results in bradykinesia and rigidity.

Monday 21 October 2013

Cerebral Cortex

  • A region of grey matter that forms the outer rim of the cerebrum
  • Consists of lots of folds, called gyri
  • Longitudinal fissure separates the cerebrum into right and left halves called cerebral hemispheres
  • Each cerebral hemisphere is split into four lobes named after the bones that cover them, so frontal, parietal, temporal and occipital lobes
  • Within each cerebral cortex are sensory, motor and association areas.

Sensory areas:

Primary somatosensory area – Located directly posterior to the central sulcus in each parietal lobe. Receives nerve impulses for touch, pressure, vibration, itch, tickle, temperature, pain and proprioception

Primary visual area – Located on the posterior tip of the occipital lobe. Receives visual information and is involved in visual perception

Primary auditory area – Located in the superior part of the temporal lobe. Involved in auditory perception

Primary gustatory area – Located in the parietal cortex. Receives impulses for taste and is involved in taste discrimination

Primary olfactory area – Located on the medial aspect of the temporal lobe. Receives impulses for smell and is involved in olfactory perception

Motor areas:

Primary motor area – Located directly in front of the central sulcus (in the precentral gyrus) in each frontal lobe. Controls voluntary contractions of specific muscles or groups of muscles (internally generated movements)

Broca’s speech area - Located in the frontal lobe only in the LEFT cerebral hemisphere. Involved in the articulation of speech eg the coordinated contractions of your speech and breathing muscles in order to allow you to speak. A stroke in this area will result in a person still having clear thoughts but unable to form words (non-fluent aphasia)

Association areas:

Somatosensory association area - Parietal lobe.
Allows you to determine the exact size and shape of an object by feeling it, determine where one body part is in relation to another, storage of memories of past somatic sensation, enabling you to recognize objects simply by touching them

Visual association area - Occipital lobe
Relates present and past visual experiences so that you can recognise what you see

Wernicke’s area - Broad region in only the LEFT temporal and parietal lobes
Allows you to interpret the meaning of speech by recognising spoken words
Stroke in this area means people can still speak but cannot arrange words in a coherent fashion (fluent aphasia)

Prefrontal cortex - Anterior portion of the frontal lobe
Personality, intellect, complex learning abilities, recall of information, initiative, judgement, foresight, reasoning, conscience, intuition, mood, planning for the future and development of abstract ideas.

Premotor areas - Immediately in front of the primary motor area
Deals with learned motor activities of a complex, sequential nature.
Generates nerve impulses that cause specific groups of muscles in contract in a specific sequence.