Neurological assessmentv1[25 10_11][1]


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Some brief anatomy and physiology and then routine for examination of Neuro system.

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  • Cerebrum/diencephalon constitute the forebrain. Divided into left and right hemispheres. Point out- Spinal cord Dorsal root ganglions Sympathetic chain ganglions Levels of spine 8,(1,2),5,5,1
  • Point out- Cerebrum Cerebellum Brain stem Ventricles
  • Broken down in next slides
  • Has a gray colour hence ‘gray matter Gray matter consists of neurons and their unmyilenated fibres White matter below consists mainly of mylinated axons interconnecting neurons
  • Located in posterior portion of the frontal lobe. Supplementary motor areas and premotor cortex believed to play a role in the planning of complex, coordinated movements Here cells are active when there is an intention to make a movement rather than during the movement itself. It deals with learned motor activities of a complex and sequential nature
  • Lesions affecting the primary somatosensory cortex produce characteristic symptoms including:  agraphesthesia , ( It is a difficulty recognizing a written  number  or  letter traced on the  palm  of one's hand after  parietal  damage.) [1   astereognosia , Patient finds it difficult to recognize objects by touch based on its texture, size and weight loss of  vibration ,  proprioception  and  fine touch   It can also produce  hemineglect , if it affects the non-dominant hemisphere. It could also reduce  nociception ,  thermoception  and  crude touch , but since information from the  spinothalamic tract  is interpreted mainly by other areas of the brain (see  insular cortex and  cingulate gyrus ), it is not as relevant as the other symptoms
  • They are situated at the base of the forebrain  and are strongly connected with the  cerebral cortex ,  thalamus  and other brain areas. Striatum- planning and modulation of movement pathways theories implicate the basal ganglia primarily in  action selection , that is, the decision of which of several possible behaviors to execute at a given time The basal ganglia play a central role in a number of neurological conditions , including several  movement disorders . The most notable are  Parkinson's disease , which involves degeneration of the  melanin -pigmented dopamine-producing cells in the substantia nigra pars compacta (SNc), and   Huntington's disease , which primarily involves damage to the striatum. [1] [5] Basal ganglia dysfunction is also implicated in some other disorders of behavior control such as the  Tourette's syndrome , 
  • Hippocampal circuit- Receives information form medial temporal lobe associated with learning and memory. Bilateral damage impairs the formation of new memories Is also damaged in dementia Amygdala- Processing of emotional responses. System responsible for fear and dread for example when walking home alone at night Also has a role in recognising other peoples emotional responses Damage may result in an inability to perceive situations as dangerous
  • Sulcus- A sulcus (pl. sulci ) is a depression or fissure in the surface of an organ, especially the brain .
  • Receives sensory info about balance, posture and limb position form the ascending tracts Compares this with information from the premotor and supplementary motor areas Acts as a comparator and if there is a mismatch it sends signals to the primary motor cortex to correct the action, producing a smoothness.
  • Contains nucleii of 11 of the 12 cranial nerves Reticular formation runs through the core of the brainstem Diffuse network of neurons which exert widespread influence on CNS functions
  • The ventricles are filled with  cerebrospinal fluid  (CSF) which bathes and cushions the brain and  spinal cord  within their bony confines CSF formed in the ventricles. The cerebrospinal fluid within the skull and spine is found between the  pia mater  and the  Arachnoid  and provides further cushioning. The Cerebrospinal Fluid that is produced in the ventricular system has three main purposes:  Buoyancy ...... CSF provided buoyancy and support to the brain against gravity. The buoyancy protects the brain since the brain and CSF are similar in density; this makes the brain float in neutral buoyancy, suspended in the CSF. This allows the brain to attain a decent size and weight without resting on the floor of the cranium, which would kill nervous tissue Protection....... the protection purpose comes into play with the meninges: pia mater, and the Arachnoid layer. The CSF is there to protect the brain from striking the cranium when the head is jolted. chemical stability.
  • Four vessels supply the brain- Right and left internal carotid arteries Sends off two branches- anterior and posterior communicating arteries Then becomes middle cerebral artery Middle cerebral artery supplies most of the surface of the brain. Anterior cerebral artery supplies medial surface of each cerebral hemisphere Branches of the vertebral arteries supply pons medulla and cerebellum Posterior cerebral arteries supply occipital and temporal lobes Two vertebral arteries
  • In most parts of the body, the smallest blood vessels, called capillaries, are lined with endothelial cells. Endothelial tissue has small spaces between each individual cell so substances can move readily between the inside and the outside of the vessel. However, in the brain, the endothelial cells fit tightly together and substances cannot pass out of the bloodstream. (Some molecules, such as glucose, are transported out of the blood by special methods.)
  • Neuropeptides are small protein-like molecules used by  neurons  to communicate with each other Oxytocin is best known for its roles in female reproduction. It is released in large amounts 1) after distension of the  cervix  and uterus  during labor, and 2) after stimulation of the  nipples , facilitating  birth  and  breastfeeding .   Vasopressin is a  peptide hormone  that controls the reabsorption of molecules in the tubules of the  kidneys  by affecting the tissue's permeability. It also increases  peripheral vascular resistance , which in turn increases arterial  blood pressure Peptides  (from the  Greek  πεπτός, "digested" from πέσσειν "to digest") are short  polymers  of  amino acids  linked by  peptide bonds . They have the same peptide bonds as those in  proteins , but are commonly shorter in length.
  • Schwann cells  supply the myelin for peripheral neurons, whereas  oligodendrocytes , specifically of the interfascicular type, myelinate the axons of the  central nervous system . The main purpose of a myelin layer (or  sheath ) is to increase the speed at which  impulses  propagate along the  myelinated  fiber. Along unmyelinated  fibers, impulses move continuously as waves, but, in myelinated fibers, they hop or "propagate by  saltation .“ Demyelination is the loss of the myelin sheath insulating the nerves, and is the hallmark of some  neurodegenerative   autoimmune  diseases, including  multiple sclerosis ,  acute disseminated encephalomyelitis ,  transverse myelitis ,  chronic inflammatory demyelinating polyneuropathy ,  Guillain-Barré Syndrome ,  central pontine myelinosis , inherited demyelinating diseases such as  Leukodystrophy , and  Charcot Marie Tooth .
  • Afferent Towards the central nervous system Efferent Away from central nervous system.
  • High ratio- One motor neuron controls many fibres Low ratio One motor neuron contorls few fibres.
  • Stimulation of patella ligament stretches the quadriceps muscle This excites the muscle spindle This then fires an action potential to stimulate the afferent nueron in the spinal cord The motor axon releases acetylcholine at Neuromuscular junction Causing muscle to contract. Biceps- C5, C6 Brachioradialis- C6 Triceps- C7 Ankle S1, S2
  • Vestibulo-ocular- e.g. For horizontal movements, lateral rectus motor neurons Cranial nerve VI are influenced by vestibular nuclei cells Medial rectus muscles cranail nerve III are driven by interneurons in the abducens nucleus.
  • Sub types of agnosia Inability to identify common objects. Inability to  draw  common objects. Inability to  copy  drawings of objects. Achromatopsia , an impaired recognition of  color . Prosopagnosia , an impaired recognition of human faces. Prosopamnesia , an impaired remembrance of human faces.
  • Nervous system Headache.....tension, migraine, subarachnoid, raised intracranial pressure, temporal arteritis. Precipitating factors Frequency Nature and location of pain Associated symptoms Timing during the day Blackout.....epilepsy, vasovagal, TIA, cough syncope, cardiac disturbances Witnesses How long did it last? What was the patient doing during the episode....shaking etc.. Any incontinence Did anyone feel for a pulse? Was there one if they did? Post blackout Immediate recovery....vasovagal Confusion and disorientation....Postictal Weakness....TIA Fits Prodrome... ‘did you have any warning you were going to blackout? Postictal period Witnesses Muscle weakness Duration Pattern of weakness Precipitating events Altered sensation distribution Change in vision Speed of onset Clarify acuity....can you read newspaper? Dizziness Need to clarify exactly what the patient means Vertigo Light headedness Postural hypotension Neurocardiogenic syncope Occurs in healthy people when forced to stand for long periods or are subject to a painful or distressing stimuli e.g. blood Arrhythmias Mechanical obstruction to cardiac output. Muzzy feeling
  • Higher function covers- Thought, memory, understanding, perception and intellect.
  • Impaired attention and orientation if acute may be associated with disturbance of conciousness If chronic is suggestive of dementia.
  • Loss of short term memories seen in diffuse encephalopathies
  • Impaired calculation usually indicates a diffuse encephalopathy Abstract thought- if interpretations are concrete this suggests diffuse encepalopathy
  • Loss indicates parietal lobe lesions
  • Prosopagnosia- bilateral temporoparietal lesions
  • All suggest parietal lobe lesions
  • ideational apraxia- lesion of either the dominant parietal lobe or premotor cortex, or a diffuse brain lesion ideomotor apraxia- suggests bilateral parietal disease.
  • Scores <25 are suggestive of dementia
  • When we want to speak, we formulate what we are going to say in Wernicke’s area which then transmits our plan of speech to Broca’s area where the plan of speech is carried out. Wernickes aphasia- People with receptive aphasia can speak with normal grammar, syntax, rate, intonation and stress, but their language content is incorrect. They may use the wrong words, insert nonexistent words into speech ( neologisms ), or string normal words together randomly ( word salad ).  Broca’s aphasia- Sufferers of this form of aphasia exhibit the common problem of  agrammatism . For them,  speech  is difficult to initiate,  non-fluent , labored, and halting. Similarly, writing is difficult as well.  Intonation  and stress patterns are deficient.  Language  is reduced to disjointed words and sentence construction is poor, omitting  function words  and  inflections  ( bound morphemes ). A person with expressive aphasia might say  "Son ... University ... Smart ... Boy ... Good ... Good ... "
  • The  arcuate fasciculus  (Latin,  curved bundle ) is the  neural pathway  connecting the posterior part of the  temporoparietal junction  with the frontal cortex While previously thought to connect  Wernicke's area  and  Broca's area , new research demonstrates that the arcuate fasciculus instead connects posterior receptive areas with premotor/motor areas, and not to Broca's area. [1] Telegrammatic speech- A simplified manner of  speech  in which only the most important  content words  are used to express ideas, while grammatical  function words  (such as  determiners ,  conjunctions , and prepositions ) and  inflectional  endings are often omitted the term  neologism  is used to describe the use of words that have meaning only to the person who uses them, independent of their common meaning
  • Extra pyramidal tract include basal ganglia, substantia nigra and cerebellum The  corticobulbar  (or  corticonuclear )  tract  is a  white matter  pathway connecting the  cerebral cortex  to the  brainstem . The 'bulb' is an archaic term for the  medulla oblongata ;
  • Extra pyramidal tract include basal ganglia, substantia nigra and cerebellum The  corticobulbar  (or  corticonuclear )  tract  is a  white matter  pathway connecting the  cerebral cortex  to the  brainstem . The 'bulb' is an archaic term for the  medulla oblongata ;
  • Extra pyramidal tract include basal ganglia, substantia nigra and cerebellum The  corticobulbar  (or  corticonuclear )  tract  is a  white matter  pathway connecting the  cerebral cortex  to the  brainstem . The 'bulb' is an archaic term for the  medulla oblongata ;
  • spastic gait   a gait in which the legs are held together and move in a stiff manner, the toes seeming to drag and catch
  • spastic gait   a gait in which the legs are held together and move in a stiff manner, the toes seeming to drag and catch
  • spastic gait   a gait in which the legs are held together and move in a stiff manner, the toes seeming to drag and catch
  • Lesions to the olfactory nerve can occur because of blunt trauma, such as  coup-contra-coup  damage, meningitis, and tumors of the frontal lobe. They often lead to a reduced ability to taste and smell. However, lesions of the olfactory nerve do not lead to a reduced ability to sense pain from the nasal epithelium. This is because pain from the nasal epithelium is not carried to the central nervous system by the olfactory nerve; rather, it is carried to the central nervous system by the trigeminal nerve (cranial nerve V).
  • Optic nerve is a sensory nerve conveying the sense of vision from the retina.
  • Fovea- Made up exclusively of cones, the fovea processes high-contrast discriminative vision (visual acuity) and colour vision. Without it, you could not see fine detail. Whereas loss of peripheral vision may go unnoticed for some time, damage to the macula will result in loss of central vision, which is usually immediately obvious. The progressive destruction of the macula is a disease known as macular degeneration and can sometimes lead to the creation of a macular hole. Macular holes are rarely caused by trauma, but if a severe blow is delivered it can burst the blood vessels going to the macula, destroying it
  • Fovea- Made up exclusively of cones, the fovea processes high-contrast discriminative vision (visual acuity) and colour vision. Without it, you could not see fine detail. Whereas loss of peripheral vision may go unnoticed for some time, damage to the macula will result in loss of central vision, which is usually immediately obvious. The progressive destruction of the macula is a disease known as macular degeneration and can sometimes lead to the creation of a macular hole. Macular holes are rarely caused by trauma, but if a severe blow is delivered it can burst the blood vessels going to the macula, destroying it
  • III (oculomotor), IV (trochlear), and VI (abducens) Horner syndrome is due to a deficiency of  sympathetic  activity.
  • Mydriatic drugs enlarge pupils Miotic drugs constrict the pupils- commonly used in glaucoma- increase the outflow of aqueous humour.
  • III (oculomotor), IV (trochlear), and VI (abducens) Observe the patient following a target up and down and to either side. Observe for diplopia or nystagmus Cover test Cover left eye, then uncover rapidly and cover right eye. Look to see if left eye has to correct to look back at your eye
  • Sensory- somatic sensation to the face Motor- muscles of mastication.
  • Sensory- somatic sensation to the face Motor- muscles of mastication.
  • Primarily motor Motor- to muscles of facial expression Parasympathetic- to lacirmal, submaxillary and sunlingual. Sensory- taste for anterior two thirds of the tongue.
  • VIII- Sensory nerve Auditory- sense of hearing Labyrinthine- sense of balance
  • Ménière's disease is  idiopathic , but it is believed to be linked to  endolymphatic hydrops , an excess of fluid in the inner ear. [15]  It is thought that endolymphatic fluid bursts from its normal channels in the ear and flows into other areas, causing damage.
  • Glossopharyngeal- Sensory- taste for posterior two thirds of the tongue, most of the oropharynx and soft palate Parasympathetic Motor- to stylopharyngeus (muscle which elevates larynx and pharynx) Vagus- Parasympathetic- visceral innervation to the heart, lungs and foregut Motor- to the larynx, soft palate, pharynx Sensory- for dura mater of posterior cranial fossa, small part of the external ear. Listen for dysphonia (altered voice production) or a bovine like cough. (associated with recurrent laryngeal nerve palsy).
  • Accessory- motor nerve supplying the sternomastoid and trapezius muscles Hypoglossal- motor nerve supplying innervation to the muscles of the tongue Weakness of scm and trap on same side- peripheral accessory palsy Weakness of ipsilateral scm and contralateral trap- umn weaknesss on ipsilateral side Unilateral delayed shoulder shrug- contralateral umn lesion
  • Glossopharyngeal- Sensory- taste for posterior two thirds of the tongue, most of the oropharynx and soft palate Parasympathetic Motor- to stylopharyngeus (muscle which elevates larynx and pharynx) Vagus- Parasympathetic- visceral innervation to the heart, lungs and foregut Motor- to the larynx, soft palate, pharynx Sensory- for dura mater of posterior cranial fossa, small part of the external ear. Listen for dysphonia (altered voice production) or a bovine like cough. (associated with recurrent laryngeal nerve palsy).
  • Inspection Posture Gait Coordination Wasting Lower motor neurone disease may cause muscle wasting Wasting is not seen in UMN disease. Fasciculation Look like irregular ripples or twitches under the skin overlying muscles at rest This occurs in LMN disease usually in wasted muscles Flick the skin over wasted muscle to try to elicit fasiculation Tremors Physiological Fine fast tremor commonly seen with anxiety, excess alcohol or caffeine. Side effect of bronchodilators Essential Slowly progressive neurological disorder. Use to be called benign essential tremor. Usually mild but can be disabling. Action Coarse and sometimes even violent. Usually associated with lesions of the red nucleus and subthalmic nucleus. Intention Is absent at rest but maximal on movement and associated with cerebellar damage.
  • Flaccidity May occur in LMN disease. Often associated with muscle wasting. Spasticity Velocity dependant resistance to passive movements A feature of UMN disease Accompanied by weakness, hyper-reflexia, an extensor plantar response and sometimes clonus. Rigidity Sustained resistance throughout the range of movement Most easily detected when the limb is moved slowly Clonus Rhythmic contractions evoked by sudden stretch of muscles When sustained indicates UMN damage.
  • Rebound phenomenon Ask patient to stretch arms out in front of them Push patients wrist quickly downwards and observe return movement Abnormal in cerebellar disorders Finger-nose test Ask patient to touch his nose and then touch your finger tip Ask him to repeat the movement as quickly as possible Heel-shin test Ask patient to slide heel of one foot down the shin of the other leg Rapid alternating movements Pat the palm of one hand with the back and palm of the other Get the patient to do the same. Abnormal in cerebellar disorders
  • James Parkinson  (11 April 1755 – 21 December 1824) [ citation needed ]  was an  English   apothecary surgeon ,  geologist ,  paleontologist , and political activist . He is most famous for his 1817 work,  An Essay on the Shaking Palsy [1]  in which he was the first to describe "paralysis agitans", a condition that would later be renamed  Parkinson's disease  by  Jean-Martin Charcot .
  • CORPUS CALLOSUM It connects the left and right cerebral hemispheres and facilitates interhemispheric communication BRAINSTEM Medulla oblongata- controls autonomic functions Cardiac Respiratory Vomiting Vasomotor Pons (bridge) Arousal Controlling autonomic functions Relaying information between the two hemispheres Sleep.
  • Visual Evoked Response (VER) : The eyes are stimulated by looking at a computer screen that is flashing checkerboard patterns of differing sizes or a strobe-type light. Usually, one eye is covered with a patch or a hand-held shield while the other eye is tested, then the process is repeated with the other eye. Some people report feeling slightly nauseated during the test, a feeling much like mild motion sickness. Brainstem Auditory Evoked Potentials (BAEP) : The hearing is stimulated by listening to test tones, beeps or clicks through headphones, usually in a dark room. Somatosensory Evoked Potential (SSEP) : The nerves of the arms and legs are stimulated by an electrical pulse delivered through electrodes stuck onto the skin, usually at the wrist or knee, but occasionally near an ankle or elbow. It feels like a small electric shock. Most people say this is completely painless, but some people find the stimulation bothersome. The presence of oligoclonal bands in cerebrospinal fluid combined with their absence in blood serum often indicates that immunoglobulins are produced in central nervous system. Therefore it is normal to subtract bands in serum from bands in CSF when investigating CNS diseases. Oligoclonal bands are an important indicator in the diagnosis of multiple sclerosis . Approximately 79%-90% of all patients with multiple sclerosis have permanently observable oligoclonal bands
  • Gabapentin is used primarily for the treatment of seizures , neuropathic pain , and hot flashes . [1] There are, however, concerns regarding the quality of the research on its use to treat migraines , bipolar disorders , and pain. [2] [ edit ] Pain Gabapentin provides significant pain relief in about a third of people who take it for fibromyalgia or chronic neuropathic pain . [3] Carbamazepine ( CBZ ) is an anticonvulsant and mood-stabilizing drug used primarily in the treatment of epilepsy and bipolar disorder , as well as trigeminal neuralgia . An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system. An example of an anticholinergic is dicycloverine, and the classic example is atropine. Anticholinergics are administered to reduce the effects mediated by acetylcholine on acetylcholine receptors in neurons through competitive inhibition. Therefore, their effects are reversible
  • Interferon beta-1a (also interferon beta-1-alpha ) is a drug in the interferon family used to treat multiple sclerosis (MS). [1] It is produced by mammalian cells, while Interferon beta-1b is produced in modified E. coli. Interferons have been shown to produce about a 18–38% reduction in the rate of MS relapses, and to slow the progression of disability in MS patients. [2] There is currently no cure for MS, though starting a course of interferons early may slow its progress. It is believed that Interferon beta based drugs achieve their beneficial effect on MS progression via their anti-inflammatory properties. Glatiramer acetate is a random polymer (average molecular mass 6.4 kD) composed of four amino acids that are found in myelin basic protein. The mechanism of action for glatiramer is unknown, although several have been proposed. Administration of glatiramer shifts the population of T cells from pro-inflammatory Th1 cells to regulatory Th2 cells that suppress the inflammatory response. [1] Given its resemblance to myelin basic protein, glatiramer may also act as a sort of decoy, diverting an autoimmune response against myelin. The symptom-causing lesions of MS are believed to be caused when inflammatory cells such as T-lymphocytes pass through the blood-brain barrier through interaction with receptors on the endothelial cells. Natalizumab appears to reduce the transmission of immune cells into the central nervous system
  • Hemianopia , also known as Hemianopsia is loss of vision in either the right or left sides of both eyes; a common side effect of stroke or brain injury
  • Hemianopia , also known as Hemianopsia is loss of vision in either the right or left sides of both eyes; a common side effect of stroke or brain injury
  • Hemianopia , also known as Hemianopsia is loss of vision in either the right or left sides of both eyes; a common side effect of stroke or brain injury Thalamic syndrome- impairment of sensory modalities on opposite side of face Choreia (or chorea ) is an abnormal involuntary movement disorder, one of a group of neurological disorders called dyskinesias. The term choreia is derived from the Greek word χορεία (=dance), see choreia (dance), as the quick movements of the feet or hands are vaguely comparable to dancing or piano playing.
  • Neurological assessmentv1[25 10_11][1]

    1. 1. Neurological AssessmentJonathan Downham Advanced Nurse Practitioner 2008Jonathan Downham 2010
    2. 2. Anatomy of Neurological System
    3. 3. The Brain
    4. 4. e
    5. 5. Cerebrum•Cerebral cortex•Basal ganglia•Limbic system
    6. 6. Cerebral cortex•Outermost to the cerebrum•Plays a key role in:•Memory•Attention•Awareness•Thought•Language•Consciousness•Movement•Folded- grooves calledsulci
    7. 7. Cerebral cortex- motor areasPrimary motor cortex-•Executes voluntarymovementsSupplementary motorareas and premotorcortex-•Select voluntarymovements
    8. 8. Cerebral cortex- sensory areasPost central gyrus-•Receives the bulk ofsensory inputs
    9. 9. Basal Ganglia•Striatum•Caudate•Putamen•Damage to striatum- Huntingtonsdisease•Globus pallidus•Substantia Nigra•Degeneration of dopamineproducing cells- Parkinsons.•Subthalmic nucleusAssociated with a variety of functionsincluding-•Vountary motor control•Learning•Eye movements•Emotions
    10. 10. Limbic system•Hippocampal circuit-•Receives informationform medial temporallobe associated withlearning and memory.•Amygdala-•Processing ofemotional responses.
    11. 11. Division of cerebral cortex.
    12. 12. Frontal lobe-•Primary motor cortex- musclemovement•Preparation of movement andcontrol of posture•Broca’s area- the ‘how’ ofspeech•Pre-frontal cortex- rich inconnections from other areas.Plan behavior, control emotionalstate.Parietal lobe-•Inputs into here build up a picture ofhow the body is positioned.•Left hemisphere represents onlyright side.•Right hemisphere represents all ofleft and some of right.•Right sided lesions will producemore severe effects on theprocessing of left half of space.•NeglectTemporal lobe-•Language comprehension andresponse- Wernickes area•Visual object recognition•Learning and memory.Occipital lobe-•Visual cortex.
    13. 13. CerebellumInvolved in-•Control of axial muscles(balance)•Coordination of head andeye movements•Control of postural muscletone and movementexecution•Controls precision in rapidand dextrous movements
    14. 14. Brain StemMedulla oblongata- controlsautonomic functions•Cardiac•Respiratory•Vomiting•VasomotorPons (bridge)•Arousal•Controlling autonomicfunctions•Relaying informationbetween the twohemispheres•Sleep.
    15. 15. Ventricles
    16. 16. Blood Supply
    17. 17. Blood-brain barrierProtects the brain from"foreign substances" in theblood that may injure the brain.Protects the brain fromhormones andneurotransmitters in the restof the body.Maintains a constantenvironment for the brain.
    18. 18. ‘Holes’ in the BBBPineal body: Secretes melatonin and neuroactive peptides. Associatedwith circadian rhythms.Neurohypophysis (posterior pituitary): Releases neurohormones likeoxytocin and vasopressin into the blood.Area postrema: "Vomiting center": when a toxic substance enters thebloodstream it will get to the area postrema and may cause the animal tothrow upSubfornical organ: Important for the regulation of body fluids.Vascular organ of the lamina terminalis: A chemosensory area thatdetects peptides and other molecules.Median eminence: Regulates anterior pituitary through release ofneurohormones
    19. 19. •Collect information fromsurrounding cells and conduct tocell body.•Principal role is to increase thepotential for synapses•Output is all or none impulse•Travels down the axon
    20. 20. •An electrical insulator•Depolarisation only occursat the nodes of ranvier•Conduction in mylelinatedneurons is approx 6 timesfaster.•Area of synapse.
    21. 21. Synapse and neurotransmitters.1. Action potentialarrives at terminalbouton.2. Depolarisationopens voltage gatedchannels3. Calcium ions enterbouton4. This liberatesvesicles5. Which then fusewith synapticmembrane releasingtheir contents6. Neurotransmitter bindsto receptors on the otherside.
    22. 22. Autonomic nervous system• Controls in voluntary internal processes e.g.-– Digestion– Regulation of blood flow• Acts mainly on-– Heart– Smooth muscle– Metabolic processes– Glandular structures.
    23. 23. Autonomic nervous system• Central control primarily by the hypothalamus– Gains information from various sources e.g.• Water status• Pain– Output in the form of• Hormonal (via pituitary gland)• Neural.– Structures in the medulla also play a role andcommunicate with the hypothalamus
    24. 24. Oculomotor nerve IIIFacial nerve VII andglossopharyngeal nerve IX
    25. 25. Spinal CordSpinothalamic tracts•Carry conscious pain, temperature, crude touch, and pressure.•Lateral and an anterior tract.•Terminate in the areas of the cerebral cortex which perceive these sensations.
    26. 26. Spinal CordSpinocerebellar tract•Carries unconscious proprioception (muscle sense) to the cerebellum•The fibres either do not cross, or cross and re-cross so that they innervate thecerebellum on the same side.
    27. 27. Spinal CordFasciculus Gracilis and Fasciculus Cuneatus (Dorsal column)•Carry discriminative touch (the gracilis) and conscious proprioception (the cuneatus).•The Fibres of these tracts go first to the medulla where they synapse and cross.•Then through a pathway called the medial lemniscus they pass to the thalamus.•Then on to the cerebral cortex for perception.
    28. 28. Spinal CordCorticospinal tract (Pyramidal tract)The corticospinal tract originates in the cerebral cortex where voluntary motor control islocalized. There are two branches, the lateral and the anterior.The lateral crosses in the medulla in an area known due to its appearance as thepyramids. Controls the precise movements of the limbsThe anterior does not cross. Control the less precise movements of the limbs Thesefibres are called "upper motor neurons" and they synapse with "lower" motor neurons inthe cord which lead to the skeletal muscles.
    29. 29. Motor Control• 3 types of movement– Reflex responses• Involuntary responses– Rhythmic motor patterns- e.g. Walking• Largely autonomic but require voluntary control tostart/stop– Voluntary movements• Goal directed, learned and improve with practice.
    30. 30. Motor Control• Sensation– Feedback control• Sense of proprioception gives us information about theposition of our bodies.• Patients who have lost this due to large fibre sensoryneuropathy do not know where there limbs are inspace unless they can see them– Feedforward control• Information is used to derive advanced informationand direct the movement toward a predicted positione.g. picking up a drink.
    31. 31. Motor Control• Upper motor neuron
    32. 32. Motor Control• Lower motor neuron– Alpha motor neurons• Production of force byskeletal muscle– Gamma motor neurons• Cause contraction ofspindle fibres– Innervation ratio• High ratio- coarsemovements• Low ratio- finemovements
    33. 33. Motor Control•Muscle fibres made up ofcylindrical structures calledmyofibrils•Action potentials sweepdown the sarcolemma•When action potentialarrives at t tubule itunblocks voltage gatedchannel•This allows outflow ofcalcium into myofibrilcytosol•This calcium is needed formyofibril contraction.
    34. 34. Motor control•Myofibrils divided by series of Z lines•Myosin- thick filaments•Actin- thin filaments•Ratchet action along muscle fibre between two filaments•At rest attachment sites are covered with troponin•Calcium binds to troponin allowing contraction- needs ATP•Relaxation occurs when calcium is removed by sarcoplasmic reticulum- needsATP
    35. 35. ReflexesTapping patella tendoncan indicate if L2 and L3are intact.May also indicate if spinalmotor neurons arereceiving an abnormaldrive from higher centres.In upper motor neuronlesions there is a loss ofdescending inhibition-therefore brisk reflexes.
    36. 36. Tone• This is the continuous and passive partialcontraction of the muscles• It helps maintain posture.• Produced by tonic firing of spinal motorneurons.• Set by stretch receptors and higher centres viathe spinal cord.
    37. 37. Control of movement•Body needs to know where it is before itmoves.•Gathers this form somatosensory,proprioceptive and sensory data•Goes to posterior parietal cortex.•This is connected with anterior frontallobe (pre frontal areas)- abstract thought,decision making, consequences ofactions.•Both send axons that converge oncortical area 6•Planning and execution of movement•Motor cortex area 4 controls musclemovement.
    38. 38. Control of movementBasal Ganglia•Selection of movement•Ensuring appropriatemovements are made-important in finemovement and walking•Control of saccadicmovement of eyes (veryfast jumps)•Memory relating to bodyposition
    39. 39. Control of movementCerebellum•Receives info from vestibularnuclei- head position•Involved in control of balance,and coordination of head andeye movements•Controls postural musclecontrol and movementexecution•Precision in rapid anddextrous movements
    40. 40. Vision•Visual field is the area which can be seenwith both eyes looking directly ahead.•Hemispheres process information from onlythe contralateral side of the axis•Each hemifield is constructed from bothretinae•E.g. Right visual hemisphere is processed inthe left visual cortex....•...but is constructed from temporal (outside)portion of the left retinae....•....and nasal (inside) portion of the right eye.•So nasal fibres cross over whilst temporalfibres do not.
    41. 41. Vision• Attention-– Active pursuit of a focus from sensory informationin order to process it further.– Pre attentive process is a rapid scanning of ascene.– The attentive process focuses on specific featuresof a scene.
    42. 42. Vision• Perception– Making sense of what is seen.– Organising visual information into objects andbackground and then identifying those objects.– Relies on comparison with memories of objects– Occurs in visual association cortex.
    43. 43. Vision• Eye movements-• Stabilisation-– Vestibulo-ocular- uses vestibular input to holdretinal image stable during brief or rapid headmovement.– Optokinetic- uses visual input to hold the retinalimage stable during sustained or slow headrotation
    44. 44. Vision• Keep fovea on target– Saccade• Very fast• Guided by current tasks• Horizontal saccadicmovements generated inthe pontine reticularformation• Vertical movements in themidbrain.
    45. 45. Vision• Keep fovea on target– Smooth pursuit• Controlled by visual and frontal corticol areas.– Vergence• Adjusts the eyes for differing image distances.• Controlled by midbrain neurons.– Smooth pursuit and saccadic eye movementscan combine e.g. When looking out of a trainwindow.
    46. 46. Vision• Agnosia-– Patients cannot recognise and name objects from visualexamination.– They may still be able to describe physical characteristicsof the object.– Failure of the higher processes of perception• Neglect-– A deficit in attention and awareness to one side of space.– Commonly related to damage in the tempero-parietaljunction and posterior parietal cortex.
    47. 47. Hearing•Once they leave the cochlearnucleus most of the axons crossover to the other side of thebrain.•Because of the bilateralprojections to the auditory cortexdamage to one side of thecentral auditory pathway will notresult in deafness in one ear.Brodmans area/ Wernickes area
    48. 48. Hearing•Pinna of outer ear crucial inlocalising sound.•Sound waves enter the ear eitherdirectly or are reflected.•Reflected sounds are slightlydelayed in hitting the tympanicmembrane.•Differences in time delay areused to determine the soundsposition.
    49. 49. Hearing•Two types of hearing loss•Conductive-•Caused by failure of sound to reach the innerear.•Sensorineural-•Caused by failure at the level of the cochleaor more centrally.
    50. 50. Somatosensation• Receptors are formed by peripheralterminations of axons of dorsal root ganglions.• Types-– Mechanoreceptors- pick up changes in pressure(touch), or movement– Nociceptors- respond to pain– Thermoceptors- temperature.
    51. 51. Somatosensation• Fibres signalling modalities of touch travel upthe dorsal column pathway.• Fibres signalling thermal and pain informationtravel in the spinothalmic tract.
    52. 52. Somatosensation•The region ofthe skininervated by adorsal root iscalled adermatome.
    53. 53. Neurological ExaminationJonathan Downham 2010•Nervous system•Headache•Blackout•Fits•Muscle weakness•Altered sensation•Change in vision•Dizziness•Tremors
    54. 54. Neurological ExaminationJonathan Downham 2010A neurological examination is composed ofthe following areas:• Mental status and speech• Gait• Cranial nerves• Motor system• Sensory system• Reflexes.
    55. 55. Mental StateAppearance and behaviour-•Signs of self neglect (depression, dementia,alcoholism).•Anxiety- restless, fidgety.•Appropriate behaviour- overfamiliar anddisinhibited, or unresponsive with little emotionalresponse•Rapid mood changes•Appropriate concern shown about symptoms
    56. 56. Mental StateAppearance and behaviour-•Signs of self neglect (depression, dementia,alcoholism).•Anxiety- restless, fidgety.•Appropriate behaviour- overfamiliar anddisinhibited, or unresponsive with little emotionalresponse•Rapid mood changes•Appropriate concern shown about symptomsMoodDelusions.
    57. 57. Higher Function• Attention and orientation• Memory• Calculation• Abstract thought• Spatial perception• Visual and body perception• Apraxia
    58. 58. Higher Function• Attention and orientation– Orientation• Time• Place• Person– Attention• Ask patient to repeat some numbers back to you• Easier if it is a number familiar to you• Make the numbers longer, then ask them to repeatbackwards.
    59. 59. Higher Function• Memory– Immediate recall and attention• Ask patient to remember an address• Or “One thing a nation must have to become rich andgreat is a large secure supply of wood.”- Babcockssentence.– Short term memory• After about 5 minutes ask the patient to recall theaddress you gave them.– Long term memory• Try to pick an appropriate event that you think thepatient should be able to recall.
    60. 60. Higher Function• Calculation– Serial sevens• Ask patient to take seven from a hundred then sevenfrom what remains and so on.• Doubling threes.• Abstract thought- frontal lobe function– Explain well known proverbs (glasshouses, rollingstone etc)– Difference between a pair of objects e.g. Skirt andtrousers.
    61. 61. Higher Function• Spatial perception (tests parietal and occipitallobe function– Clock face- ask patient to draw a clock face and fillin numbers. Then ask him to draw a particulartime.– Five pointed star – ask them to draw a fivepointed star– Half clock missing- visual inattention– Unable to draw- constructional apraxia
    62. 62. Higher Function• Visual and body perception- parietal andoccipital lesions– Abnormalities of perception of sensation despitenormal sensory perceptions are called agnosias.– Facial recognition- ask patient to identify famousfaces (prosopagnosia)
    63. 63. Higher Function– Body perception• Patient ignores one side and is unable to find his handif asked• Does not recognise his hand if shown it(asomatagnosia)• Unaware of weakness of affected side (anosagnosia)• Ask patient to show you his index ginger, ring fingeretc. (finger agnosia)• Ask patient to touch his right ear with his left indexfinger (left/right agnosia)
    64. 64. Higher Function– Sensory agnosia• Pt closes eyes. Place familiar object in hand and askwhat it is (astereognosis)• Write a letter/number on his hand and ask what it is(agraphaesthesia)• Apraxia– Ask the patient to perform an imaginary task• Unable to initiate even though understands- ideationalapraxia• Performs but makes errors- ideomotor apraxia
    65. 65. Neurological ExaminationJonathan Downham 2010• Speech• Aphasia• Dysphonia• Disturbance of voice production.May reflect abnormality of thenerve supply via the vagus.• Dysarthria• Motor disorder. Can reflectdifficulties at different levels.
    66. 66. Neurological ExaminationJonathan Downham 2010• Aphasia- absence of speech• Wernicke’s aphasia-• Poor comprehension,fluent, (receptive) butoften meaningless• Broca’s aphasia• Preservedcomprehension, nonfluent (expressive)speech• Global aphasia• Difficulty understandingand speaking.
    67. 67. Neurological Examination•Test speech•Aphasia•Listen to patients speech, fluency and contents•Assess their comprehension by giving simple commands•Assess their ability to name objects•Assess their ability to repeat sentences, (No ifs, ands orbuts).Type Lesion Speech fluency Speech content Comprehension AssociationExpressive Brocas area non-fluent normal normaltelegrammatic speech,dysarthiaReceptive Wernickes area fluent impaired impaired neologisms, excessive speechConductive Arcuate Fasiculus fluent normal normalimpaired function inrepetitive tasksGlobal Parietal lobe/ dominant hemisphere non-fluent impaired impairedcontralateral visual/sensoryinattention, defects inwritten language
    68. 68. Neurological Examination•Test speech•Dysphonia•In dysphonia speech volume is reduced and voicesounds husky.•May be due to recurrent laryngeal nerveweakness.•May have bovine like cough- cough lacksexplosive start- ? vocal cord palsy.•Ask patient to say ‘eeee’- if weakens may indicatemyasthenia
    69. 69. Neurological Examination•Test speech•Dysarthia•Ask the patient to repeat ‘British Constitution’,‘West Register Street’, and ‘baby hippopotaumus’•Cerebellar dysarthia- slurred speech. (?MS)•Extrapyramidal dsyarthia- soft and monotonous(Parkinsons)•Pseudobulbar dysarthia- high pitched withstrangled quality•Bulbar dysarthia- speech has a nasal quality.
    70. 70. Neurological Examination•Test speech•Dysarthia•Lower motor neuron dysarthia-•Palatal- nasal speech as with bad cold- Xcranial nerve•Tongue – distorted speech, letters t,s andd- XII cranial nerve•Facial- difficulty with b,p,m and w- VIIcranial nerve
    71. 71. Gait• Ask patient to walk up and down the room• Observe– Posture– Pattern of arm and leg movements• If gait appears normal ask them to walk heelto toe.
    72. 72. GaitHemiplegic gait•Ipsilateral arm held flexed andadducted•Ipsilateral leg held extended•Pts tilt pelvis forward to swingaffected leg aroundSpastic gait•Pts walk in small steps•Legs are held in adduction withknees touching each other•Gives the gait a scissored quality
    73. 73. GaitParkinsonian gait•Slow and shuffling•Small stride length•Reduced arm swinging•Flexed postureFootdrop gait•Pts over flex theknee and hip•Gives a highstepping qualityCerebellar ataxic gait•Pts walk on a wide base•Often unsteady•Stagger to affected side ifunilateral lesions•Stagger backwards if bilaterallesions•Appear drunkRomberg test•Ask patient to stand with feettogether•Pts with cerebellar or vestibularlesions are ataxic with eyes open•Pts with proprioceptive sensoryloss may be ataxic when they closetheir eyes.
    74. 74. Neurological ExaminationJonathan Downham 2010The Cranial Nerves.Once On October TheTenth, All Five Virgins GaveVictor A Hug.Some say marry money but mybrother says big brains mattersmost
    75. 75. Neurological ExaminationJonathan Downham 2010The Cranial NervesI- Olfactory- smell- sensoryII- Optic- sight- sensoryIII- Oculomotor- sight- motorIV Troclear- sight- motorV- Trigeminal- face/jaw/cornea- sensory and motorVI- Abducens- eye- motorVII- Facial- sensory and motorVIII- Vestibulocochlear - sensoryIX- Glossopharyngeal- mouth- sensory and motorX- Vagus- speech- sensory and motorXI- Accessory- spinal accessory- motorXII- Hypoglossal- speech and tongue- motorOnce On October TheTenth, All Five Virgins GaveVictor A Hug.Some say marry money but mybrother says big brains mattersmost.
    76. 76. Neurological ExaminationJonathan Downham 2010I- Olfactory nerve-•Not tested routinely.•May only wish to test if the patientcomplains of being unable to smell.•This should then be tested by askingpatient to close his eyes and one nostriland then exposing him to an aroma.•Bilateral loss of sense of smell is oftenassociated with loss of sense of taste
    77. 77. Neurological ExaminationJonathan Downham 2010II- Optic Nerve•Visual Acuity•Visual Fields•Fundi
    78. 78. Neurological ExaminationJonathan Downham 2010Visual Acuity•Test with Snellen chart•Hold chart about 20feet away.•Test both eyes gettingpatient to cover eacheye in turn.•Ask patient to readsmallest line possible
    79. 79. Neurological ExaminationJonathan Downham 2010Visual Acuity•Correctable reduced acuity =ocular defect•Un-correctable reduced acuity =•Corneal lesion•Cataract•Macular degeneration•Retinal heamorrhage•Optic neuropathy•Bilateral occipital lesions
    80. 80. Neurological ExaminationJonathan Downham 2010Visual fields-Check for visual inattention-Hold hands stretched out halfway betweenyou and patientMove each hand separately then togetherAsk patient to indicate which moved.•Tested using confrontation•Sit at same level as patient.•Ask them to cover one eye•You cover opposite eye.•Bring finger into view from allangles.•Patient to say when he sees it.
    81. 81. Neurological ExaminationJonathan Downham 2010Fundi-•Using ophthalmoscope•Lower lights•Start at +20 setting•Hold scope in left hand toleft eye when looking atpatients left•Patient to focus on spoton wall behind you.•Swap for other side.
    82. 82. Neurological ExaminationJonathan Downham 2010Cotton wool spotsresult from occlusionof retinal pre-capillaryarterioles supplyingthe nerve fibre layerwith concomitantswelling of local nervefibre axons.Flame-shapedheamorrhage inassociation with severehypertensionPapilloedema frommalignant hypertension.There is blurring of theborders of the optic diskwith hemorrhages
    83. 83. Neurological ExaminationTypes of eye movement•Saccadic (Frontal Lobe)•Rapid movement of one point of fixation to another•Pursuit eye movement (Occipital Lobe)•Slow eye movement used to maintain fixation on a movingobject•Vestibular-positional eye movements (Cerebellar vestibular nuclei)•Eye movements which compensate for movement of the head tomaintain fixation•Convergence (Mid-brain)•Movements that maintain fixation as an object is brought closerto the face.
    84. 84. Neurological ExaminationJonathan Downham 2010III (oculomotor), IV (trochlear), and VI (abducens)Look at eyelids forptosis and symmetry•Common causes•Congenital•Horners syndrome•III nerve palsy•Myasthenia gravis
    85. 85. Neurological ExaminationJonathan Downham 2010III (oculomotor), IV (trochlear), and VI (abducens)Test the pupillaryreflex by shining alight on the pupil.Look at both directand consensualresponse
    86. 86. Neurological ExaminationJonathan Downham 2010III (oculomotor), IV (trochlear), and VI (abducens)Observe the patientfollowing a target upand down and toeither side.Perform cover test, looking forsquintCover left eye, then uncoverrapidly and cover right eye. Lookto see if left eye has to correct tolook back at your eye
    87. 87. Neurological ExaminationJonathan Downham 2010III (oculomotor), IV (trochlear), and VI (abducens)
    88. 88. Neurological ExaminationJonathan Downham 2010V- TrigeminalSplit into threedivisions
    89. 89. Neurological ExaminationJonathan Downham 2010V- TrigeminalSensory- test the sensation over the three distributionsof the nerve using cotton wool and pin.Corneal reflex- lightly touch the cornea with dampcotton wool. Patient should blink•Afferent defect (Vth cranial nerve defect) results indepression or absence of direct and consensual reflex•Efferent defect(VIIth cranial nerve defect) results inimpairment or defect on affected side.Motor- test jaw opening against resistance.
    90. 90. Neurological ExaminationJonathan Downham 2010VII- Facial•Patient to look up- note any loss ofwrinkling•Patient to close eyes. Try to gentlypull them open.•Ask patient to bare teeth. Look forany asymmetry.•Ask patient to blow out cheeksLook for asymmetry of nasolabial folds and position of two corners of mouth.If weakness detected then if confined to lower part of face- UMN lesionIf both upper and lower them LMN lesion
    91. 91. Neurological ExaminationJonathan Downham 2010VIII- Vestibulocochlear nerve•Whispered voice test-•Stand behind patient with mouth about 15cmfrom ear to be tested•Mask hearing in other ear by rubbing tragus•Ask patient to repeat what you say.•Move away to arms length. If patient can hearwhispered voice from here then hearing is said tobe normal.
    92. 92. Neurological Examination• Webers test– Place fork inmiddle offorehead– Ask patient wherethey hear sound.– Normally thiswould be equallyin both ears or inthe middle.– Note to whichside it lateralises.Jonathan Downham 2010
    93. 93. Neurological Examination• Rinne’s test– Place the vibratingforks base againstthe mastoidprocess– Then place the forkat the externalauditory meatusand ask which islouder.– Air conductionshould be betterthan boneconductionJonathan Downham 2010Sensorineural deafness i.e. Air condction betterthan bone conduction;•Lesion of the cochlea e.g. Menieresdisease•Lesion in the nerve
    94. 94. Neurological Examination• IX and X- Glossopharyngeal and Vagus– Ask patient to say ‘aah’ and observe for palatalmovement. Make sure it is bilateral.– Observe uvula. Should stay central.• Moves to one side- upper or lower motor lesion of vagus on theother side• Does not move on saying aah- bilateral palatal muscle paresis– Only test gag reflex if thought necessary.– Listen for dysphonia (altered voice production) ora bovine like cough.Jonathan Downham 2010
    95. 95. Neurological Examination• XI and XII- accessory and hypoglossal– Force chin down against resistance of your hand– Turn the chin to one side against resistance– Ask patient to stick out their tongue• Observe for any fasiculations or wasting• Note any deviation to one side or the other.Jonathan Downham 2010
    96. 96. Neurological Examination• XI and XII- accessory and hypoglossal– Small tongue• With fasiculations-bilateral lower motor neurone disease, motorneuron disease• With reduced speed of movement- bilateral upper motor neuronedisease– Tongue deviates to one side• With unilateral wasting and fasiculation- unilateral lower motorneurone disease• With normal bulk- unilateral upper motor neurone disease– Tongue moves in and out on protrusion (trombonetremor)• Cerebellar disease. Jonathan Downham 2010
    97. 97. Neurological Examination• Motor system– Inspection– Palpation– Assessment of muscular tone– Assessment of tendon reflexes– Assessment of power– Assessment of coordination– Assessment of gait.Jonathan Downham 2010
    98. 98. Neurological Examination• Upper motor neuronedisease affects thosemotor neurons whichoriginate in the motorregion of the cerebralcortex.• Lower motor neuronedisease affects thosemotor neuronsconnecting thebrainstem and spinalcord to muscle fibres.Jonathan Downham 2010
    99. 99. Neurological Examination• Five patterns of muscular weakness-Jonathan Downham 2010Upper motor neurone (UMN)•Increased tone•Increased reflexes•Pyramidal pattern of weakness•Weak extensors in the arm•Weak flexors in the legLower motorneurone (LMN)•Wasting•Fasiculation•Decreased tone•Absent reflexesMuscle disease•Wasting•Decreased tone•Impaired or absent reflexesNeuromuscular Junction•Fatiguable weakness•Normal or decreased tone•Normal reflexesFunctional weakness•Normal tone•Normal reflexes•No wasting•Erratic power
    100. 100. Neurological Examination• Inspection– Posture– Gait– Coordination– Wasting– Fasciculation– Tremors• Physiological• Essential• Action• IntentionJonathan Downham 2010
    101. 101. Neurological Examination• Palpation– Complete exposure of the patient. Maintaindignity– Look for:• Asymmetry• Deformities• Wasting• Fasiculation– Palpate muscles to feel their bulk.Jonathan Downham 2010
    102. 102. Neurological Examination• Tone– Upper limb• Hold patients hand as if shaking hands. Support elbow and putthrough a range of movements– Lower limb• Roll leg from side to side then briskly lift knee into flexed position– Decreased tone- heel does not lift off the bed– Knee clonus• With leg extended sharply push patella with thumb and forefinger– Ankle clonus• Support patients leg with knee and ankle in 90 degree flexion.Quickly dorsiflex and evert the ankle.Jonathan Downham 2010
    103. 103. Neurological Examination• Tone:– Resistance felt by the examiner when moving a jointpassively through its range of movement.• Flaccidity– May occur in LMN disease. Often associated with musclewasting.• Spasticity• Velocity dependant resistance to passive movements• A feature of UMN disease• Accompanied by weakness, hyper-reflexia, an extensorplantar response and sometimes clonus.• Rigidity• Sustained resistance throughout the range of movement• Most easily detected when the limb is moved slowly• Clonus• Rhythmic contractions evoked by sudden stretch of muscles• When sustained indicates UMN damage.
    104. 104. Neurological Examination• Deep tendon reflexes– Using tendon hammer allow weight of tendonhammer to determine strength of blow– Abnormally brisk reflexes are generally a sign of uppermotor neurone disease– Diminished or absent reflexes are signs of lowermotor neurone disease– If no response try reinforcement methods• For upper reflexes ask patient to clench teeth• For lower reflexes ask them to hook their fingers togetherthen try to separate.Jonathan Downham 2010
    105. 105. Neurological Examination• Reflexes can be graded-0 = absent+/- = present but only with reinforcement1+ = present but depressed2+ = normal3+ = increased4+ = clonusJonathan Downham 2010
    106. 106. Neurological Examination• Biceps jerkJonathan Downham 2010Nerve: musculocutaneous nerveRoot: C5, C6
    107. 107. Neurological Examination• Triceps jerkJonathan Downham 2010Nerve: radial nerveRoot: C7
    108. 108. Neurological Examination• Brachioradialis/SupinatorJonathan Downham 2010Nerve: radialRoot: C6
    109. 109. Neurological Examination• Knee jerkJonathan Downham 2010Nerve: femoralRoot: L3-L4
    110. 110. Neurological Examination• Ankle jerkJonathan Downham 2010Nerve: tibial nerveRoot: S1-S2
    111. 111. Neurological Examination• Plantar reflexJonathan Downham 2010A normal reflex is for the patientto have plantar flexion of all histoes.A completely abnormal reflex isindicated if there is-• dorsiflexion (turning upward)of the big toes,•fanning of all toes,•turning upward of the ankle,• or flexion (bending) of theknee and hip.
    112. 112. Neurological Examination• Power can be graded-0 = no movement1 = flicker of muscle when patient tries to move2 = moves, but not against gravity3 = moves against gravity but not against resistance4 = moves against resistance but not to full strength5 = full strengthJonathan Downham 2010
    113. 113. Neurological Examination• Assessment of power• ShoulderJonathan Downham 2010Abduction Muscle: deltoidNerve: axillary nerveRoot: C5
    114. 114. Neurological Examination• ElbowJonathan Downham 2010ExtensionFlexionFlexionMuscle: biceps brachiiNerve: musculocutaneous nerveRoot: C5, C6ExtensionMuscle: tricepsNerve: radial nerveRoot: C7
    115. 115. Neurological Examination• WristJonathan Downham 2010ExtensionFlexionExtensionMuscle: radialis longus, brevis andulnarisNerve: radial nerveRoot: C7FlexionMuscle: Flexor carpi radialisNerve: medial nerveRoot: C6,C7
    116. 116. Neurological Examination• FingerJonathan Downham 2010Extension FlexionAbduction AdductionMuscle: extensor digitorumNerve: posterior interosseousRoot: C7Muscle: Flexor digitorum superficialis andprofundusNerve: median and ulnaRoot: C8Muscle: first dorsal interosseousNerve: ulnarRoot: T1Muscle: second palmar interoseousNerve: ulnarRoot: T1
    117. 117. Neurological Examination• HipJonathan Downham 2010Abduction AdductionExtension FlexionMuscle: gluteus medius and minimusNerve: superior gluteal nerveRoot: L4,L5Muscle: adductorsNerve: obturatorRoot: L2, L3Muscle: iliopsoasNerve: lumbar sacral plexusRoot: L1, L2Muscle: gluteus maximusNerve: inferior glutealRoot: L5, S1
    118. 118. Neurological Examination• KneeJonathan Downham 2010FlexionExtensionExtensionMuscle: quadriceps femorisNerve: femoralRoot: L3, L4FlexionMuscle: hamstringsNerve: sciaticRoot: L5, S1
    119. 119. Neurological Examination• AnkleJonathan Downham 2010DorsiflexionPlantar flexionPlantar flexionMuscle: gastrocnemiusNerve: posterior tibialRoot: S1DorsiflexionMuscle: tibialis anteriorNerve: deep peroneal nerveRoot: L4, L5
    120. 120. Neurological Examination• Assessment of coordination– Rebound phenomenon– Finger-nose test– Heel-shin test– Rapid alternating movementsJonathan Downham 2010
    121. 121. Neurological ExaminationJonathan Downham 2010Sensory examination•Light touch•Dab with cottonwool•Pain•Check patient canidentify stimulus assharp.
    122. 122. Neurological ExaminationJonathan Downham 2010Common peroneal nerve Femoral nerveLateral cutaneous nerve
    123. 123. Neurological ExaminationJonathan Downham 2010Vibration sense•Place tuning fork on sternum and ask if he can feelit•Patient then closes eyes•Place on distal joint and ask if he feels it.•If not move up to next proximal joint•Compare left with rightJoint position sense•Move the distal interphalangeal joint of the indexfinger/toe by the sides•With patients eyes closed ask them if the joint ismoving up or down.
    124. 124. Parkinson’s Disease.• Caused by cell death in thesubstantia nigra– Basal ganglia normally exert an inhibitoryresponse on various muscles.– This prevents them becoming active atinappropriate times.– When an action is required dopaminereduces this inhibition.– So low levels of dopamine function demandgreater exertions for any given movement
    125. 125. Parkinson’s Disease.• Hypokinesia-– Poverty of movement e.g. Lack of blinking, expressionlessface.• Bradykinesia-– Slowness of movement. Initially manifests as problemswith performing fine motor movements.• Akinesisa-– Difficulty initiating and termination movements• Rigidity-– Caused by increased muscle tone. Can be uniform (leadpipe) or ratchety (cogwheel).• Rest Tremor-– Maximal when limb is at rest, disappearing with voluntary
    126. 126. Multiple SclerosisDemyelination affecting white matter tracts in the centralnervous system• relapsing-remitting: clearly defined disease relapses with full recovery or withsequelae and residual deficit upon recovery; periods between relapsescharacterised by a lack of disease progression. About 80% have relapsing-remittingdisease at onset● secondary progressive: initial relapsing-remitting course followed by progressionwith or without occasional relapses, minor remissions and plateaux. About 50% ofpeople with relapsing-remitting MS develop secondary progressive MS during thefirst 10 years of their illness● primary progressive: disease progression from onset with occasional plateaus andtemporary minor improvements allowed. About 10–15 % have primaryprogressive disease at onset.Marked variability in disease progression.
    127. 127. Multiple Sclerosis• Areas of demyelination are found in the whitematter of the brain and spinal cord.• There is a particular predilection for lesions incertain areas-– Periventricular areas of the cerebral hemispheres– Corpus callosum– Brainstem– Cervical cord– Optic nerves
    128. 128. Multiple SclerosisClinical featuresOptic and retrobulbar neuritis•Subacute visual loss•Usually unilateral•Central scotoma•Pain on movement•Afferent pupillary defectBoth pupils dilate whenswung to the affected eyeBrainstem presentation•Diplopia- failure of adduction ofthe eye•Nystagmus-due to cerebellardisease•Vertigo•Dysartia•Facial numbness•Dysphagia•Ataxia•Hemisensory or patchy sensorychanges in the limbs.Spinal cord lesion•Spastic paraparesis•Tetraparesis•Tonic spasms•Difficulty walking•Sensory loss
    129. 129. MS- diagnostic tools• Evoked potential studies– Visual– Somatosensory– Brainstem auditory evoked potentials• CSF sampling– Presence of oligoclonal bands• MRI scan
    130. 130. MS- Treatment• Treatment for MS can be split into three maincategories:– treatment for relapses of MS symptoms (steroids)• Methylprednislone- reduce immune response and swelling aroundnerves– treatment for specific MS symptoms• Visual problems- gabapentin• Muscles spasms/neuropathic pain-physio/gabapentin/carbemazapine• Mobility problems- mainly muscular-physio and drugs as above• Depression- anti-depressants• Bladder problems- over active bladder needs anti-cholinergics-oxybutynin or tolterodine
    131. 131. MS- Treatment– treatment to slow the progression of MS (disease-modifying medicines)• Interferon beta 1a and 1b• Glatiarmer• Natalizumab
    132. 132. Stroke (CVA)Middle Cerebral Artery Occlusion•Most commonly artery involved in stroke.•Supplies motor and sensory cortices•Comprehension (Wernickes) and expression(Brocas)•These areas are found in the dominant hemisphere•So an occlusion in the left cerebral artery will affectspeech production in right handed individuals•Contralateral hemiplegia•Contralateral corticolhemisensory loss•Dominant hemisphereaphasia•Non dominanthemisphere neglect•Contralateral hemianopia
    133. 133. Stroke (CVA)Anterior Cerebral Artery Occlusion•Occlusion proximal to anterior communicationartery normally well tolerated because of cross flow•Distal occlusion causes•Contralateral weakness•Corticol sensory loss in the leg•Incontinence is often present•Contralateral grasp
    134. 134. Stroke (CVA)Posterior Cerebral Artery Occlusion•Effect of occlusion depends on site•Proximal occlusion- III nerve palsy,contralateral hemiplgia, thalamic syndrome,chorea•Corticol vessel occlusion- hemianopia withmacular sparing•Bilateral occlusion- corticol blindness- pt isblind but lacks insight and often denies it.
    135. 135. Myasthenia GravisAutoimmune disorder•Antibodies directed against postsynaptic acetylcholine receptors•Results in weakness and fatigability ofskeletal muscle groups.SymptomsOcular- ptosis and diplopiaCranial muscles- weak face and jaw-dysarthia-dysphonia-dysphagiaLimb weakness -usually proximal-shoulder and hipsAxial weakness -neck and trunk-respiratory muscle