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neuro paper - estionl" I I I 12 6IIy1I old woman...

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Unformatted text preview: estionl' '- ' -" - I I I 12 6IIy1I' old woman presents to Your office with hgr 11115111111111.5133 complaining of'1Bins . . You find out'fmm a further consultant that they Were very Pime‘i ““11 your quick ' ._ 111d needles in her toes and feet and also" 1 and hands. Bother .questiOJJiilg _ - - I ', . refer”! “seeing that the above neurological Ifindmgs we” all refined Igiven _tIhB' din-Ck ' - W 4151th use of. alcohol, however in the last year 513331333 I‘ .- ' I intervention I' I lrarnaticall}r reduced the amount she drinks 11m; from her doctor. regarding a ' - - ' ' ' 3) H w d 3 this ew [If h , I . . o oe n 1 ormauon c ange your 1113 oars. attIy liver. - I _- I I z . _. - I . how this occurs . ' ‘ gm " ' Dracuss 'the diagnosis and Sin _35m_m_fi0“1 you find that there rs aI stbcldn' - araesthesia. There 13 some Iwealm'ess ' - _ .. _ . = — - - - :— ———-—- I -- _ ‘ '- Posteralateral “139555 133 a PEER-931V? degeneration of posterior and lateral col11111ns_ 7" ___I_ m- .. ____. I_I.Ef_the_spi11a1 eerd, sometimes with degeneration oftbe Eight-1131' nerves. It' 15 'a co—mglieafign of pernicious anaemia caused by nutrititmal defici'eoc 1111 I and other forms ofI anaemia. . I ”_ “—‘h—y s es(v1tamin B12} 1) was: is your oment 1151‘ of differential diagnosis Alcoholic peripheral neuropathy . I Diabetes mellrtus U190 WW 4) What was the. likely from of' n'eatruem that they administered to this pafiBmI 11111 .' : ' . ' - ' - ‘ — Postero'lateral sclerosis_ . , I V1tam1nB121nJecaons I I _ WM: 1111112,er (ESQ-5115' I1. . ,? 0945’ 011' 1:3 A few weeks later the patient returns to your clinic with her husband She' now has. - ' - I I I33 g Emmi excessive tiredness _fan' bility and 1s breathless on' enertion. Her husband mentions that ‘ - . ‘ Iflthlt are flit“- presenting Symptoms Of Delin'um Ima. nitial Symptoms include ' es. Examnnmon at this time reveals loss of. test '1: es closed 5111-11.33: is some broadening of Wslight personality. gosition sense, posinvIe I-Loss of appetite, insomnia and general restlessness followed by agitation, I excitement, disorientation; mental confusion, vivid and often frightening the base while walking and 10880 W YOUJR‘JW .- 1931‘??? ‘5 now 55% ICGCM'G 3 - hallucinations acute fear and anxiety 111111113 (1 d l I voluntary mnscle wealoiess.I' 1- creased lower limb DTIRIT '1. some Ispasnoior of the I hands feet legs and to 'e fever Ificfm 11 1111;111:115 coarse tremor oéthe 11 .__ , hear m e clue perspiratiom I BXtI‘Cl'IIlifiCSI Mixed 013W :3 lOW. ‘ 0379311311011 0!: . ' distress and precordia'l pain . ‘ 1:13.135; 2) Discuss her current symptoms Al oussI '11}teI neIIIurol 031 :11 symptoms in more? regards to the areas and or tracts of the nervous system Kn affected Excessive tiredness Fatigability, Bresthless on SKIEIUQID IKJI 191-. fiffij ,2 muWI SEEM: ' . . Personality changes . - I I. Doss ILposifion sense ' ' '- Positiv'e Romb'erg a test ' eyes closed only- tlus indicates a loss éfijoint po'srtion sense, Cerebellar syndrome _DOI’EQl CQllo What are the 4 characteostictype s of riphei'al neur o a ‘ .' 1) Axons! arriving back mwwgedom‘ mwgbflfics 2) Demyelinaring' Mr” or new (”We WW W' 3) Chrome, often hereditary W161 4W“? SJ l l I ' 4j Vascular [ngéorrl'b'l .113an tilt-M Area safer traet Frontal lobe 11:1- Iii-e refrontsl area an 1 I‘ . Quoshon 2 - . A 44 year oldII woman was brought to a olini by her husband who gave a history of I diso dis 'viItl an; etfuluess“ These symptoms had become more severe in the latst several months The patient had reCentIl‘y. begun to complain of headaches and after shI hand what she descnbed as i‘a'fit”, her husband insisted she see a doctor my 1 l , a i N W mi" Wit: '- I Guiqr :- ‘m mills Card, I I eurolog1c e lion shOIWed apathy_ and difficulty focusion attention, impairment, of l l memory; left papilledema, facial asymmetry, lack of moevemnt on the light sidhe 'of_tl1e facen and general weakness but synnnen'ic Ireilexes' 1n the remainder of the body; All EEG showed an abnormal slow wave focus :1 the left hemisphere. Imaging Studies showed a calcified multifocal mass in the left frontal Iregiou. 1311._1ao$%. W 1.1111113 - -. actress / I lest Watt 91511101 lobe 4/ What 1Is the differehti'al diagnosis” with justification based on the above I Chm: Min ' - findings (210m 1am. 3.508113% Mental impairment (disorientation, confusion; 'stzactibility. and partial loss 'memory)I . .sugg'est a lesion in one or both frontal lobes; The right face signs made a left sided- lesion propable and was confirmed IIvvith BEG_anI_d'1n1aIging studies The seizures also- - I- suggest an irriative lesion“ 111- or near the motor cortex. _ - Consequently, difl‘ereudal diagnosis included a intracranial 11111110111“, an atypical chronic infection (Without history of fever} or In degenerative disorder I ' —__A _brain biopsy was performed and a _diag11_osis._ B] .the- next 111,111; patient had become _ ___ _ __ — ' comatosed dilated fixed pupils and she died soon afterwards. Biopsy, findings include' small hemorrhages inIhe brain stem and extensive pathologic changes in the forebrain. Iii) What happened after the brain biopsy The biopsy procedure chub‘ibuted to a progressive inhacranial haemorrhage which lead to brain herniation and death iii) What is the most likely diagnosis Malignant glioma Question 3 Numerous hypostheais and theoretical models concerning how the vertebral sublimation _I may cause nerve interference exist Discuss some of the current theories and research that leads to theirI' support How the vertebral suhluxation may cause nerve. interference 15 described by hyposthesis and theoretical models. Neurological theories of the subluxation describe how the suhluxat'ton' influences the nervOus system. There are three main theories describing how . ' joint sublu'nadon is thought to influence function These theories purpose include i) Intervertebral foreman IVF encroachment . ii) Altered somatic sensory input - ' iii) ' - Spinal cord distortion IVF encroachment Most widely accepted . I I I Clinical literahrre abounds that encroachment of nburnl structures within the NF my produce pain and parathesia as well as changes in muscle tone and autonomic activity ' Asssumpfions: - Pressure on contents of the “NF will either increase or decrease neural activity .' -' Increased neural activity produces parenthesis, pain, hypertonic muscles, I' _'vasoconstriction and sweating - .. I ' While decreased neural hcfivity produces numbness, muscle weaknesslpal‘a-lyma vasodilafion and dry skin - . Altered Somatic sonscry input The {VP encroachment theory can ’tapply to joints lacking IIVF such as (3911 C112 the sacroiliac or extremity joints. Clinical experience suggests that chiropractic adjustments often bring clinical improvements in the absence of demonstrable encroachment within; . . the IVF Basic research dembnstrates significant somatic sensory and motor responses tr altered articular afferent input. Changes are reported 111 nociceptrye and kinaesthetic . sensibilities, muscle tone, deep tendon reflexes, joint mobility and sympathetic activity Noxious stimulus is known 11'; suppress low threshold mechanoreceptor activity. It has _;..'_.'___..-..ubeen established that lbw sensory input. to despinal cord inhibits nocicepfive pathtvay's: _‘1._.———-Cousoqently, noxious sfimultiscf spinalstrucmresrunybe expected to introduce ' _ nocioeptor input while suppressing low threshold sensory input, and simultaneously - decreasing the normal inhibition of the nociccptive pathways within the cord. Seaman refers to this potent combination as diSafierentation. Therefore, clinical and basic I research investigations suggest an important altemafive to the NF encroaohrdent theory. Spinal cord distortion Gnostic relates two mechanisms be which the dentate ligaments may adversely influence the conduction of neural impulses within the spinal cord: 1} ' _Direct mechanical irritation via Identato ligament traction and ii) Venous occlusion and resultant local blood stasis and ischemia ofI the upper cortical cord1 also produced by dentate ligament traction. Grostic observenathat the strength of the demote ligaments 111 the upper cervical region and the dynamics of the cervical spine lengthening on flexion, contribute to the - possibility of spinal cord (listens with upper cervical misahgnment _ Referring to the work of Briog',‘ he notes there' is an approinrrmtclyn 3mm chango' in cervical spinal canal length fromfull extension to full flefionI Dora] attachments to the ' foranien magnum and possibly to the axis and atlas are also used. He ostii'nahes that an average lateral misalignment between the skull and atlas of three degrees “fill produce approximately 3mm lateral displacement of the atlas. ’I'his 31111111211331 displacement' 1s ' '-approximately 23% of the total width of the spinal cord inthe upper cervical region ‘ (approximately 13m). A recent Isgudy corroborates the argument that cord:distract10n could produce a conduction block. Jarzem reported decreased spinal cord blood flow an. concurrent interruption of somatdsenspry evoked potcnfials following experimental cord distraction A study by Emery underscores the mechanical strength and immobilizing ' character ofthe upper cervical dentate ligaments“ Emory relates numerous case of - . potential necropsy that demonstrates fatal kinking of the medull'a— —spinal c'ord junction' In hydrocephalic children due to the interaction of a freely moveablebram stout and afixed upper cervical cord (fixed via string dentate ligament attachment) Question 4 'I I. A 5.1 lffiah old female presents with a 35yr history of headaches They Commenced when .. she was appropmately 16 years of age and continued for 10 yr after which may 51153913331341 for the cunt 15yrs They have been present on and off for the last Syrs but I- I for the 13-3 two years they have been increasingly severe Apart from he'adaeheI her od1e1 I - catches it early' - . a: has...“ a; .-I‘ reflexes and gait - jot. symptoms are nausea and vomiting with the headache She its; ltiey are not 'I ' ' related to her mefisiral tIiycIe 'II'Ille only medication she takes'I is for the unguided if she ' - Curie. COW. i).DDx_I I. I-I w‘chr gHfiII _ '- Ciassicmigraine - LSOL ng - 'I Cluster headaches - .‘ MenopausalI ' " SOL I. ° Cervicogenic heafiache—-——.—._.. . __ - I ii) What are the first 6 questions you would ask 1) Whfiils the pain like . - . I ‘ '2) Whenisthepain- — -. 3) Where-isthbpain ' ' 4) Aggravating factors 5) Relieving factors - 6)I Do you nofice if there are anypi‘ecipitafing causes iii} I What examination would you perform Examination _ Observation: does the padent look sick or well - people with migraine or tension headaches usually look well between attacks Those with terminal arteritis, brain tumour or other serious headaches often look sick even when they do not have a headache '- Is there evidence of psychopathology . - ' 301136 state they are in the midst of an agnosing headache, looking all the while quite well and even oh occasions sniileing. Other evidence of psychological disturbance may include overt depression, anxiety or hypochOHdrosis IPaIlpafim‘a: is there tenderness of exhacranial structures such as scalpa‘rteries- scalp or - neck muscles or sinuses,_ etc: acme} site of pain, temporal arteries, suboccipizals and muscles of mastication ‘ -' findings of tenderness. of éxItracraniaI tissues snggest that the headache emanams . ‘ from these structures This 111 not always a benign adulation howevcri temporal . arteiidsI is an summon headache that is dangerous . ' .wu-LI-AT wide-Weak»- condiment, visual fields, pupils, primed Full cervical ROM, distraction, comicssion, ken-1'- . ' Vitalsan‘dcardiac . I ' that include hurhbuess ofthcrsiderofface for the last two years is important in relieving stress also. viewed with concern pardcularijf in a_ I ' _---'atienIt headaches of recent onset A 55y: old male presents with s- chronicallysfiffneclt. He has been getting headaches—I Neurological consultation Iwhich included MRI and CT- .of brain. Endoscopic examiatior and a battery of blood tests revealed no absennality‘ orfinds beyond nonnal limits.- The: has been non trauma to the head or neck The patient is £1de investigator and under considerahle stress His plain .x— —rays show surprisingly little degenerative changes and a well preserved cervical cine. Howeverhis general range of motihn is poor and his I paraspin'al muscles are tense, painful and fibrotIic 1)I HIyou were to proceed to cervical adjustments \vhart techniques. if any, would yo use to manage (both before and after the adjusunent) the propfiodeptii'e and ncciceptive Status of this man’ s cervical spine Before adjusting: soft tissue work on trapezius. levator scapulaeI and posterior cervical muscles. Perhaps he needs to get a weekly massage prior to his adjushncnt's. - Lengthening and stretching. of the. cervical musculature and shtmlder muscles (ie serratu. a-nterior)’ 1s necessary to improve this' mans posture and therefore symptoms Decreasing stress at work and ensuring adequate sleep and nutrition to combat this stress. Eiercisin 2) You may use flow charts to demonstrate the diagnostic and management plan foi this patient ' . Question 6: A 50351- old male accoumant presents with a six week hintiry of right sided leg pain of- I I .' obscure onset He engages in no sporting activities. There is weakness of his right extensor halluces longusI muscle and a loss of sensation in the doisum of his right foot. _ His right SILR 1s painful at 50 degrees. He ocoasionally has pain on coughing. but " sneezings is always painful in his lumbar region i} What nerve is most likely involved ' LIS- leppijes extender hIallicus longus and dorsum of the foot ii) Where 1s it most liltelyI to be affected II Lumbar spine helmeen W5 IVD as SLR positive at % $5: iii) . What funcdonal elements of the nerve have been influmccfi Sgfigory and motor 1 I '- iv) What spinal cord reflex mechanism will have been influenced Sin-etch reflex for L5 'wijl be diminished leading to atmphy war v- v) _ What fourfactors will most strongly influence his prognosis _. . . . 'I - Correct diagnosis - - . _ - flfjb . - 1 Potholes}: 0!? the. L651911____:_ - ._ - .. .n. -.____.s.-.I... . - .- : Patient compliance with seamlenh . _ - _ _._..__..____I_- _ . Whether or not the patient does things to aggravate his condition Question 7 41yr old man With progressive weakness and unsteadiness in his legs, heghn more than one. year earlier with 'creeping' and tingling feelings 1n his feet. Developed burning? on soles of feet; the rest of his feet became numb 'His legs had became so Weak an? had bogunto stumble. For about six months he had tingling in his finders and hands, his fingers felt clumsy. Lost more than 6kg Heavy smoker and drinker. Wtofii . 1 What are your immediate concerns about this caseIL 6} Dro‘d ss‘r-awol lhimanégMMi-W ”ML W‘s} WlLosSI 1; \JlLGES My: I th c any other information you require from the histog; .. We at 1’??de {£75414 ,‘onuvII' M; 4:" at; w {5" str— fi/ij) gs“ £1“ mi famine 31 or? Low «f M’MM W11 t examinnnon would you perform on this patient_ . _ ,- fifiimo, uperlriuo XI nu ma. W' fifilfl mfljd Neurological examination Poorly muscled with conspicuous atrophy in the c'alves and forearms. Weakness of - movement in both ankles and wrists and slightly weakened _movenmntof the knees and . elbows. High stepping gait. Loss of touch and pain on feet, distal third of legs and on the hands and diets] halves of the forearm giving a glove and stocking distribution of sensory loss. Soles of feet and calf- muscles were hyperalgesic when squeezed. 'Anlrle and biceps . reflexes were absent and kneejerks and triceps reflexes were diminished i)' Where are the lesions. _Gi've eiudenIcIe to support . Alcoholic peripheral neuropathy - Begins with burnings mainly” 1n lower eittremities ' . Patient may present with weakness 6 Poor proPfiDCeption- stumbling I - ' Affects the cerebellmn midline— broad base gaite Dying back phe'nomenon— distal to proximal 3‘ Muscle wasting is trident 1n axonal but absent in demylinafing neuropathy Generally syrnmetripal ususally starting distally inrhe lower limb and spreading to Iuppe‘r limbs in a similar matter before aspending to proximal muscle groups Alcoholic peripheral neuropathy‘ is most likely due to nutritional deficiencies, it is characterised as annual degeneration with segmental demyelinalion ' Large myelinated- carry propriocepfion and vibration, signs and $yn1ptoms inplude pins and needles (parass'thesia) and loss of JDl‘flt position sense ' 'r ' Small unmyeiiuated- can-y pain and temperature, signs and symptoms include. burning .- _ sensation—said loss (if—pain Infill-temperature sensation - Lesion is in-the - - "_heral nerve axon With associated demyelination ' Multipl(pherail_ nerve are damaged making this a polynemopathy Both sensory an- motor fibres have been affected This loss of sensation andniotor function' ma gloVe and missing distributioa is due- to the dying baclr. phenomenon whereby nerve axons degernate from ' distal (initially) to proximal (as the disease progresses) - - Polyneuropathies are non-selective when it enmes to nerve fibres are affected and therefore both large Iuyeiinated and small unmyelinated fibres are equally insulted This Is' ndted' 1n the histo He recall symptoms beginning lyr. earlier' in his feet v'vrth tingling feelings I {paracsithesia}; This progressed within 61111113 to the same feeling In his fingers and hands with associated progress in the lower limbs (bunting pains . in soles offset), rest of feet numbness. Weakness of his legs can be explained by the involvement of motor fibres III the peripheral nerve I-lis gait is unstead due to loss of proprioception fibres' 1n the posterior white column or destination of the corehelIll'Jm which IS responsible for (so-ordination of rnovomonts Apart fromloss of funchou. there are also positive findings of polynemopatbies. These include hyperal'gesia and a burning sensati on— poaitive for small myelinated fibres,- as well as pardthesia—I posifiye for large m elinatedfibres. All aredetailed 1n the Irish) '- ' -- -- -:‘ _ Muscle wasting' 1s evident of axonal degeneration also and is evident in this patients conspicuous atrophy 1n clavs and forearms - miles: are will result in a loss of Urn _' ii) What' re the diagnosis, what 1s the basis for this oondition Alcoholic peripheral neuropathy. Tbis' 1s charactefiselby a burning sensation 1n the feet, I decreased DTRS, muscle atrophy and motor and sensory loss, all which are pronentin " this pelican This condition is amibutable to the excessive eonsumptionof alcohol (nutritional defi oiency) ' PIICA versus ALGA ...
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