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El Dolor

¿ Como se trata el dolor musculo-esqueletica y desarollar su conocimientos clinicos?

de Martin Krause

Master Applied Science (Manipulative Physiotherapy)

Graduate Diploma Health Science (Exercise & Sport)

Graduate Certificate Health Science Education

Bachelor Applied Science (Physiotherapy)

Contenido

- Introducion

- Inflammacion Neurogenica

- Ganglio de la raiz dorsal

- Disminuacion de los umbrales

- La moderacíon del dolor en la médula espinal

- Hiperalgesia secundaria en el periferico

- Areas de la modulacion del dolor

- El foramen intervertebral

- Impulsos ectopicos

- La hiperalgia secundaria en la medula espinal

- El Placebo y Nocebo

- La Historia Actual y Pasada

- Examen subjectivo (El processo del razonamiento clinico)

- Los mecanismos de regulacion/modulacion del dolor y de la inflamacion

- La relacion entre los nervios somaticos y sympaticos

- La modulacion desendiente de los centros superiores

- Centro-alrededor inhibicion

- Centros superiores en la modulacion de los emociones

- La importancia del razanomiento clinico

- Allostasis

- Sarcopenia y systema immuna

- Tratamiento

Introducion

Para el paciente y para el kinesiólogo, el origen del dolor es frecuentemente difícil de localizar.  Por lo tanto es difícil encontrar un tratamiento específico cuando la causa del problema no es claro. Hay varias razones para esta situación, pero principalmente son dos:

· la primera son múltiples dimensiones del dolor

· la inexactitud del kinesiólogo durante el proceso del razonamiento clínico.

Para efectuar un razonamiento cognitivo/mental, el kinesiólogo necesita conocimientos de anatomía, neurofisiología, biomecánica, patología, aprendizaje motor, y conocimientos clínicos.  Además de estas cualidades de conocimiento, la selección y aplicación de las técnicas son el resultado de su actitud y habilidad.

A: Neurofisiología del dolor localizado

Hay dos factores en la herido/lesión musculo-esquelética.

1. Trauma en el tejido blando y a veces los huesos.

2. Inflamación neurogénica y no-neurogénica.

La inflamación neurogénica es la reacción de los nervios durante la modulación y recuperación de la inflamación.  La inflamación no-neurogénica es la reacción de los vasos sanguíneos y los componentes sanguineos.  Esta diferenciación es meramente ilustrativa, como una forma de entender el mecanismo del dolor.  El sistema simpático periférico controla el orden de la cascada de reacciones inflamatorias entre el sistema nervoso y la sangre.  Al mismo tiempo el sistema simpático periférico tiene una funciona enlazada con el sistema inmunitario (figura 1).

Figura 1a: La conexión entre el ganglio de la raíz dorsal (DRG), el sistema simpático periférico (SNS), el sistema inmunitario (PGI2, PGE2, Leucotrienos) y substancias inflamatorio (substancia P, histamina, bradikininas). .

Figura 1b: Modulacion de los nervios periferios

Demasiado NGF -> hiperalgesia Insufficiencia del NGF -> dolor neuropatica

(Adaptado de Blottner & Baumgartner 1994; p236: McMahon 1996. IASP Congress del Dolor, Vancouver)

La consecuencia de la inflamación es una disminución de los umbrales de los receptores nerviosos no solamente con participación en la transmisión de información nociceptiva, sino también, los nervios que normalmente transmiten informaciones no dolorosa (figura 2).

Figura 2: Disminución de los umbrales de los receptores nerviosos

Significativamente, la disminución de los umbrales de los receptores tiene una consecuencia importante para la modulación del dolor en la médula espinal. En principío, el concepto de compuerta del dolor indica que los impulsos dolorosos son modulados por impulsos no dolorosos (figura 3).  Por ejemplo el sobarse alrededor el lugar doloroso después de un trauma como un golpe ó quemando del pelo. Sí, hay una disminución de los umbrales este proceso no funciona!

Figura 3: Portas del dolor en la medula espinal.  Las fibras tipa II (A-beta) pueden inhibir los impulsos en las fibras III/IV (A-delta, C) vía los neuronas con rango amplio (WDR=wide dynamic range) sobre los neuronas noci-especifico (NS)

Cuando hay edema a causa de la extravasación de los vasos sanguíneos o restricción linfática, hay una tendencia a una acumulación de una 'sopa inflamatoria'.  Si este edema esta en un compartimiento o área cerrada, siguiendo esta acumulación, habrá una mayor  disminución de la irrigación que comprometerá el metabolismo en las fibras mielinizadas del tipo II.  Consecuentemente, la disminución de la velocidad de la conducción de los impulsos eléctricos produce un compromiso de la función de las vías/compuerta del dolor, provocado por un retraso de los impulsos en las fibras tipo II (en la medula espinal) en relación a los impulsos de las fibras tipo III/IV, lo que provoca una hipersensibilidad del tejido blando.

Es posible que este edema sea la consecuencia de la inflamación del trauma en el tejido blando (ej: los ligamentos longitudinales, la duramadre, y el disco intervertebral).  Es importante destacar que la inervación del tejido blando proviene de múltiples niveles de la columna vertebral a través de  los nervios sinuvertebrales (figura 4).  Notablemente, esto significa la posibilidad que la transmisión de los impulsos nociceptivos existe en más de un nervio que produce hiperalgesia neurogénica secundaria.

Figura 4: Multiples niveles de inervación del tejido blando.  Por ejemplo, una herida en el nivel L4 tiene también inervación de los niveles vecinos (L3, L5).

Incluso es posible observar un compromiso del ganglio de la raíz dorsal (DRG) en el foramen intervertebral.  Este compromiso puede generar  'impulsos ectópicos' a la periferia y a la medula -  en ambos direcciones!  Entonces, puede producir inflamación neurogénica e hipersensibilidad en cada dirección; en la periferia y en la medula (figura 5).

A veces se produce 'dolor neuropatico' especialmente cuando hay desmielinizacion del nervio o impulsos excesivos en el sistema simpático.

Figura 5: Impulsos ectópicos pueden producir inflamación neurogénica y hipersensibilidad en la periferia y en la medula.  Notan que el nervio sinuvertebral (SNV) es un nervio periférico con una inervación en el foramen intervertebral (IVF) y el canal espinal.  El SNV tiene una mezcla de las fibras del sistema somático y simpático.

Aparte de las múltiples inervaciones que podrían producir un aumento de la hipererlgia secundaria, cuando hay impulsos eléctricos nociceptivos suficientemente intensos, las neuronas de la medula espinal distribuirían estos impulsos a neuronas vecinas. Esto es posiblemente para evitar una sobrecarga de acividad eléctrica en la neurona, que podría destruiría.  Particularmente las neuronas WDR están involucradas en este proceso (figura 6).

Figura 6: Las neuronas de amplio rango distribuirían los impulsos eléctricos a las neuronas vecinas para evitar un daño a la neurona.  El efecto es un aumento del área dolorosa y de la hiperalgesia secundaria.   Sí este mecanismo no funciona, es posible llegar a 'dolor neuropatico'.

NS= nociceptive specific = Nociceptiva especifica

WDR= neurona dinámica amplio rango (wide dynamic range)

B: Neurofisiología del dolor en los Centros Superiores

Como es posible que el cerebro localice estos impulsos? Comúnmente, el paciente puede decir dónde está el dolor más intenso. Pero hay veces en que el dolor en el brazo o en la pierna es más intenso que el dolor en el sitio de la patología de la columna. En estos casos es importante preguntar al paciente donde empezó el dolor.  Esta posibilidad existe en la historia clínica actual (figura 7).

En ciertos casos las neuronas vecinas tienen hipersensibilidad a causa de un daño o una herida anterior.  Estas neuronas pueden encontrarse hasta lugares cuatro niveles anatómicos arriba y abajo de la inervación del problema actual.  Entonces un problema en la historia pasada puede ser importante en el proceso del razonamiento clínico.  Eso debido a la neurofisiología.

También, hay factores de 'dinámica inversa' (inverse dynamics) de la biomecánica pueden tener importancia para hacer un diagnostico y un plan de tratamiento.  Por ejemplo un daño o lesión en el tobillo puede cambiar la manera de caminar (el poder de la extensión, disminuir  la flexión dorsal) lo que produciría alteraciones en el ritmo de la pelvis y la columna (leer  'gait' & endurance training ).  Pero también, se sabe que problemas en la columna puede aumentar la rigidez o la debilidad en los músculos de la pierna. En el razonamiento clínico es importante que el kinesiólogo tome un decisión acerca de que elemento es más importante en la cronicidad del problema: la causa inicial o el efecto que ha tenido ( la causa de la causa).

Sí no se tratan todos los elementos estableciendo una prioridad, es difícil para paciente y terapeuta mantener la dirección de los objetivos del tratamiento.

Figura 7: El proceso del razonamiento clínico. No se ha incluido en este diagrama ciertos examines especiales como por ejemplo técnicas de energía muscular 'muscle energy techniques' , 'dry needling', technicas especiales para el examen del pelvis, etc...... (miran muscle energy & pelvis y también la rodilla y taping )

De esta manera es posible hipotetizar múltiples enfoques de tratamiento (working hypothesis).  Por ejemplo, un dolor en la pierna puede ser un problema localizado o puede tener origen en la columna. La interacción con el paciente facilita determinar las características del dolor en las actividades cotidianas. Utilizando las repuestas del paciente se puede analizar sí la carga se encuentra en la pierna misma o  principalmente en la columna.  Estos procesos de razonamiento inductivo y deductivo se utilizan para confirmar o rechazar la hipotesis.

C: Cuales son los mecanismos de regulación/modulación del dolor y de la inflamación?

Hay por lo menos cuatro mecanismos para la regulación/modulación del dolor y inflamación

  • · sistema nervioso simpático periférico (figura 8)

Figura 8: La relación entre los nervios somáticos y simpáticos. Generalmente el sistema simpático puede disminuir la inflamación vía extravasación en los vasos sanguíneos y interacción con el sistema inmune. Este ejemplo es del nervio sinuvertebral, pero todos los nervios periférico tienen un innervación simpático.

  • modulación descendente (figura 9)

Figura 9:  La modulación de descendente desde los centros superiores puede prevenir la propagación de los impulsos hasta los centros superiores, y también puede controlar el espasmo reflexogenica probablemente en colaboración con el sistema simpático.

  • Centro-alrededor inhibición (figura 10)

Figura 10:  Centro-alrededor inhibición para localizar el sitio de dolor e inflamación:

Da un foco para el sistema nervioso vía inhibición y aumento de la actividad WDR y NS para determinar el sitio donde se necesitan inflamación y recuperación.

WDR = wide dynamic range = neurona dinámica amplio rango

NS = nociceptive specific = Nociceptiva especifica

  • Centros superiores (figura 11)

Figura 11: Centros superiores pueden controlar las emociones y las reacciones del sistema motor y sensorial en la periferia vía la modulación en los varios centros superiores y modulación descendiente en la medula.

Haga un 'click' sobre los varias 'hotspots' en la diagrama para navegar a mas informaciones. Conocimientos sobre conocimientos para construir pensamientos profundos a consecuencia del 'pain matrix' (matriz del dolor)

 

D: La importancia de la neurofisiología para el razonamiento clínico

Es muy probable que 'la irritabilidad' (figura 7) sea un reflejo, no solamente de los umbrales de los receptores (figura 2), sino también de los mecanismos de modulación.  En estas ocasiones preguntarle al paciente cuales actividades causan el dolor y cuales actividades alivian el dolor.  Al preguntarle como le afecta el dolor durante la noche se demuestra no solamente el grado de inflamación pero también la habilidad cognitiva para soporta el dolor.

Con análisis psicométrico se puede obtener información sobre sus motivaciones, emociones, y igualmente la severidad del problema.  ¿Cuales son los factores sico-sociales con importancia en la manera como se maneje el problema?

La historia previa y actual ofrecen la oportunidad de analizar los factores anteriores y subsecuentes que inhiben la resolución del problema.

Es importante establecer un sistema de cuantificación para evaluar el efecto de las técnicas seleccionadas para el manejo del problema.  Por lo tanto se nececista un proceso para evaluar el éxito de su tratamiento.  El éxito confirmará o rechazará la hipótesis original (working hypothesis). Esta evaluación puede ser realizada al observar los siguientes factores: la intensidad del dolor, la duración del dolor, la distribución del dolor, que actividades aumentan o disminuyen el dolor, cuantas veces el dolor despierta, cuánto tiempo se necesita para dormir, y por cuánto tiempo hay rigidez en la mañana ........etc.

¿Que son los factores en el salud que facilitan la recuperación y cuales factores prohíben resolución? ¿ Existen problemas con el peso ( f figura 12) , con sarcopenia y el sistema inmune ( figura 13 ) o hormonal (figura 14)?

Figura 12: Sobrepeso pone una carga inmensa sobre las articulaciones, pero poco peso causa susceptibilidad en el sistema inmune.

Figura 13: Los músculos tienen importancia para las cargas biomecánicas cotidianas, pero también las proteínas de los músculos son importantes para el sistema inmune. El buen uso de la insulina depende en el funcionamiento de los músculos.

Figura 14: Condiciones como fibromyalgia son aspectos  que requieren consideración en los examines subjetivo e objetivo. Quizá un daño en la nuca debido a un accidente automovilista en la historia previa tiene significancia para una disfunción de los ganglios simpáticos del sistema nervoso periférico. Tambien el sistem immuno usando los musculos. En principio el poder immune esta una consecuencia del actividad oxidativia en el mitochondrio y possiblemente el desplacamiento del fascia dentro los musculos (mirado con ultrasonido) reflejen ni solamente el estado mecanica pero la funciona metabolica tambien.

E: Tratamiento

El tratamiento sigue el examen. Es importante establecer un plano para manejar el examen físico. Dentro de este plano hay expectaciones de cuales estructuras están afectadas y cuales son factores significantes en la cronicidad del problema. Adicionalmente se incluye disminución o aumento del poder muscular que contribuyen a la continuación del problema. Se mira la posibilidad de demasiado 'force closure' en los músculos globales y disminución de control de  coordinación entre los  'estabilizadores específicos (locales). Como es la transmisión de fuerzas entre una parte del cuerpo y la otra (inverse dynamics).  Hay 'form closure' donde las articulaciones tienen congruencia?  ¿Hay espasmo e inflamación?  ¿Cual es el grado de la inflamación?  ¿Está el problema en una etapa de resolución o aumento? ¿Que es la causa de la causa? (Figura 15).  Aportan sus hipótesis de trabajo a más o menos probable.

Figura 15:  Análisis de la historia previa y actual en adición a toda la otra información provisto por el examen subjetivo pueden servir como guías en las decisiones tomadas durante el periodo de evaluación del éxito del tratamiento.

Un ejemplo del dolor somático en el examen objetivo y formulación de los dibujos clínicos con razonamiento clínico

 

Dos ejemplos del notación en casos del dolor radicular en el examen objetivo

Un ejemplo de un tratamiento usando conceptos de neurofisiología y biomecánica se encuentran en la sección de Mechanical Traction donde es posible aumentar 'el ambiente' dentro el foramen intervertebrales con cambios en los dimensiones del foramen que podrían mejorar el irrigación (sobre todo a los vasos sanguíneos, incluyendo el plexos de Batson).  Puede ser un mecanismo para aumentar la regulación de inflamación neurogénica en la periferia (incluido el nervio sinuvertebral de la columna) (Figura 16).

Figura 16: Un hipótesis del modulación neurogénica del ganglio de la raíz dorsal es un aumento de los dimensiones el foramen intervertebral con tecnicas manuales y el otro son modulación de los centros superiores vía el sistema simpático periférico y modulación descendiente.

Figura 17: Hay multiples lugares en el cerebro donde las impulsas electricas a consequencia del calor nociceptivo son transmitado

Figura 18: Anticipacion del dolor affectado la experienca del dolor donde expectaciones formen la realidad.

Figura 19 : Este expectaciones son aplicable para tratamiento. Entonces es importante que la terapeuta comprenden la percepcion de efficaz atraves todo el razonamiento clinico - de narativa actual, razonamiento inductivo y deductivo, historia pasada (hipersensibilidad neurogenica a consequencia del heridos anteriores y memorias del dolor), y la historia actual (mejorando, peorando, arreglando activo o passivo).

Figura 20: Expectaciones del menos dolor tienen una influencia significante sobre la actividad neuronal en el cerebro.

Figura 21: Anticipacion - Memoria - Emociones - Planificaciones

 

F: Conclusiones

Cualquiera manera de eficaz, los centros superiores son envueltos en los procesos de percepción y reacción. Regulación del espasmo y contracion-relaxacion del los músculos para manejar la coordinación en la zona neutra son importante.  Vale poco cuando se mejorar el dolor sin ejercicios para evitar que ocurra nuevamente el mismo problema o otro problemas con la misma causa (por ejemplo hiperflexibilidad y muy poco  'form closure', hipoflexibilidad' y excessiva 'force closure').

Figura 22 :  Miran el pagina sobre el pelvis y 'muscle energy techniques'

El problema con 'fisicalismo' como discutado de Cahana es que 'nosotros no somos mas que nuestro sinapsis' ("eliminativo") o 'somos ultimamente nuestro synapsis' ("reductivo" o "simbolico").

"Nuestro consciente esta en un estado de "intencion" que significa que si exploramanos el estado de mente alrededor el percepcion del dolor se resultaron en intenciones conductuales que no sean suficientes, porque el mente cambiarse en concordencia con los consecuencias intencionales de los percepciones sensoriales". Se significa que nuestro sistema sensorial esta controlado del mente y todos las relaciones existenciales de la realidad son una consequencia del "constructivismo". Nuestro valores y los valores del paciente son los mediantes que nosotros entendemos y la observadora y el observante son interdependiente que ofrecan la accomodacion del multiples realidades que formaran el total.

Cahana (2007) concluido con una declaracion que "no puedo separar dolor de la persona sufriendo la experienca del dolor, y no puedo omitar la experienca humano en las explicaciones scientificas sobre como se funciona nuestro mente. Entonces un nuevo subjectivismo, interpretivismo, fenomenolgia esta necesario para captura la complexidad de la narativa experiencado del paciente (dyad narrativa)".

Para la terapeuta el razonamiento clinico puedo establecer un camino para encuentrar una filosofia de estar que se cambiaron su propria vida y la vida de los clientes atraves el desarollo de los conocimientos mas profundos.

Una explicación de la importancia de aprendizaje motor existe en el sección sobre Avoidance of Injury & Expertise in Orienteering

Explicaciones precisas y referencias (en mi lengua preferida) sobre dolor y inflamación neurogénica existe en el sección Pain & Inflammation

Miran Razonamiento Clínico para más explicaciones y 'un link' al ejemplos clínicos son al fin del sección de 'instructional design'

Sobre todo el proceso del razonamiento clínico es una posibilidad para encontrar nuevos dibujos clínicos y también identificar problemas en sus propias conocimientos teoréticas y clínicas.

Dolor e Inflamación: un abordaje Neurofisiológico y el Razonamiento Clínico en la Dosificación y en la Terapia Manual (PDF)

Energia Muscular - exploracion (Pdf) (Castellano)

Energia Muscular - valoracion (Pdf) (Castellano)

Razonamiento clinico (Pdf) (Castellano)

Emociones (Pdf) (Castellano)


 

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  • Thu 14 Sep 2017

    Cervical Spine implications in concussion

    Neck aetiology, autonomic and immune implications, exercise and diet in the musculoskeletal physiotherapy management of Post Concussion Syndrome (PCS) by Martin Krause, MAPA, Titled member Musculoskeletal Physiotherapy Association of Australia  A 14 year old boy presented to A&E, in August 2016, after receiving an impact to the head during AFL (Australian Rules Football). Although his SCAT3 scores were relatively mild, he went on to suffer severe lethergy, resulting in a lengthy abscence from school, culminating in a return to school for exams in the first week of December 2016. Even by December, even a 30 minute walk was extremely fatiguing. To place this into perspective, he had been playing elite academy grade AFL for several seasons and was an extremely fit outdoor adventurer. Confounding Variables : end of season injury and hence no follow up from the academy suffers from Hypermobile Joint Syndrome (HJS) and possibly Ehlers Danlos Syndrome (EDS), however Beighton score 4/9. suffers from food intolerances, particularly to Glutin and diary, but also some other foods. Potential IBS and autoimmune issues. had just gone through a growth spurt (190cm) Imaging : Brain MRI normal Medical Examination : Balance remained impaired to tandem walking and single leg stance. The vestibular occular motor scale showed significant accomodation deficit of 15cm and there was a mild exacerbation of symptoms. ImPACT testing revealed adequate scores and reaction time of 0.65 which is within acceptable range. History : School holidays December - January. Return to school and was placed in the lower classes. Prior to his concussion he was a top 10 student at an academically selective high school. Took up basketball and rowing as summer sports. Academic results tanked. Several Basketball injuries (Feb - April 17') as a result of what apppeared to be muscular imbalances from the relatively recent growth spurt, as well as taking on a new sport. Showed little interest in returning to AFL as no-one had followed him up during the previous year.  Current History : September 2017 showed a continued decline in academic levels. School teachers noted an inability to concentrate. Academic results still well below pre-concussion levels. Fatigue continuing to be problematic.  Literature Review : Post Concussion Syndrom (PCS) is defined as "cognitive deficits in attention or memory and at least three or more of the following symptoms: fatigue, sleep disturbances, headache, dizziness, irritability, affective disturbance, apathy, or personality change"  Further complications of PCS also appear to be an increased risk of musculoskeletal injury Nordstrom et al (2014, BMJ Sports Med, 48, 19, http://bjsm.bmj.com/content/48/19/1447) Predictors of PCS are uncertain. However, the following clinical variables are considered factors at increasing risk. These include prior history of concussion, sex (females more prominant), younger age, history of cognitive dysfunction, and affective disorders such as anxiety and depression (Leddy et al 2012, Sports Health, 4, 2, 147-154). Unlike the 'good old days' which recommended a dark room and rest for several weeks post concussion, the consensus appears to be a graded return to exercise in order to restore metabolic homeostasis. Incredibly, highly trained young individuals can find even exercises in bed extremely demanding. Kozlowski et al (2013, J Ath Train, 48, 5, 627-635) used 34 people 226 days post injury to conclude significant physiological annomalies in response to exercise which may be the result of 'diffuse cerebral swelling'. Researchers have noted lower systolic and higher diastolic blood pressure in PCS (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Due to autonomic dysfunction manifested in altered cardiovascular and pulmonary responses (Mossberg et 2007, Arch Phys Med Rehab, 88, 3, 15-320) some clinicians have recommended the use of the exercise program for POTS (Postural Orthostatic Tachycardia Syndrome). This is a 5 month program which recommends mainly exercise in the horizontal and sitting positions for 1-4 months, including recumbent bike, rowing ergometer and swimming laps or kicking laps with a kick board. Month 4 upright bike and Month 5 upright training such as a elliptical trainer or treadmill.  http://www.dysautonomiainternational.org/pdf/CHOP_Modified_Dallas_POTS_Exercise_Program.pdf Other progressive exercise therapies have also included 20 minutes per day, 6 days per week, for 12 weeks of either treadmill or home gym exercises at 80% of the heart rate at which their concussion symtoms are exacerbated. Their programs were individually modified as the heart rate provoking symptoms increased. When compared to the 'control group', this intervention was shown to improve cerebral perfusion on fMRI, increase exercise tolerance at a higher heart rate, less fatigue and were showing activation patterns in areas of the brain on performing math processing test which were now normalised (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Graded exercises could also have included 'motor imagery' as espouse by the NOI group and the work of Lorrimer Moseley (University South Australia) when dealing with chronic pain. Ongoing Symptoms : The literature review by Leddy et al (2012) found that ongoing symptoms are either a prolonged version of concussion pathophysiology or a manifestation of other processes, such as cervical injury, migraine headaches, depression, chronic pain, vestibular dysfunction, visual disturbance, or some combination of conditions. Physiotherapy Assessment : One year PCS, fatigue continued to persist. Cognitive deficits with school work were reported to becoming more apparent. Assessment using various one leg standing tests employing oscillatory movement aroud the hips and knees for kinetic limb stability and lumbopelvic stability, which had been employed 6 months previously for his Basketball injuries were exhibiting deficits, despite these being 'somewhat good' previously. Physical Examination : cervical and thoracic spine Due to the Joint Hypermobility Syndrome (JHS) it was difficult to ascertain neck dysfunction based on range of movement testing. ROM were unremarkable except for lateral flexion which demonstrated altered intervertebral motion in both directions. Palpation using Australian and New Zealand manual therapy techniques such as passive accessory glides (upslopes and downslopes and traction) exhibited muscles spasms in the upper right cervical spine. In particular, the right C1/2 regions demonstrated most marked restrictions in movement. Eye - Neck proprioceptive assessment using blind folds and laser pointer also  revealed marked variance from the normal. Repositioning error using the laser pointer with rotation demonstrated marked inability to reposition accurately from the left, tending to be short and at times completely missing the bullseye. Gaze stability with body rotation was NAD. Gaze stability whilst walking displayed some difficulty. Laser pointer tracing of the alphabet was wildly inaccurate. Thoracic ring relocation testing also revealed several annomalies, which may have also accounted for some autonomic dysfunction.  Occulomotor assessment and training Upper Cervical Spine : The upper cervical spine (atlas and axis) represents approximately 50% of the available rotation. An investigation into the environmental and physiological factors affecting football head impct biomechanics found that rotational acceleration was one of the few factors approaching significance and concluded that more research should be undertaken to evaluate this (Mihalik et al 2017 Med Sc Sp Ex, 49, 10, 2093-2101). Headache : Commonly referred to as cervicogenic headaches, one in five headaches in the general population are thought to be due to the cervical spine. The Upper Cervical Spine is particularly vulnerable to trauma because it is the most mobile part of the vertebral column, with a complex proprioceptive system connecting the vestibular apparatus and visual systems. It also coincides with the lower region of the brainstem and fourth ventricle. The brainstem houses many neurones associated with autonomic responses to pain and balance. Imaging of the fourth ventricle for swelling of the 'tonsils' and Arnold Chiari malformations are recommended when symptoms persist. In particular, children and adolescents are more vulnerable to neck contusions due to the proportionately larger head and less developed musculature. Cervical vertigo and dizziness after whiplash can mimic symptoms of PCS.. Mechanoreceptor dysfunction and vertebrobasilar artery insufficiency should be part of the differential diagnosis. Mechanical instability of the Upper Cervical Spine should also not be missed. Cervicogenic Headaches Further Interventions : Neurocognitive rehabilitation of attention processes. Psychological intervention using cognitive behavioural therapy (CBT). Neuro-opthalmologist to assess and treat smooth pursuit eye tracking. Naturopath for food intolerances and dietician for the optimisation of diet. Diet :  In cases with chronic fatiguing factors, nutrition can be become a vital aspect into the reparative process. This may include energy and mineral rich foods such as bananas, green leafy vegetables for iron and magnesium (200-300mg), oranges for vitamin C (anit-oxidant and helps with the absorption of iron), anti-oxidant rich foods such as EPA/DHA (1000mg) fish oil, curcumin (tumeric), Cats Claw, Devils Claw, Chia seeds, fruits of the forest (berries), and CoQ10 with Vitamin B. Folate and Ferritin levels should also be checked. Calorific energy intake should balance with energy exependiture. However, as we are often dealing with young individuals, as in this case, some form of comfort food may be appropriate such as, nuts, legumes, homus and sushi. Protein intake prior to carbohydrate intake may help ameliorate any blood suger fluctuations due to Glycemic Index factors, however simple carbohydrates (high GI) should be avoided wherever practical. Even oats need to be soaked overnight and cooked briefly, otherwise they become a high GI food and may even affect the absorption of iron. The type of rice used can also influence GI, hence the addition of protein such as fish. Protein supplementations are generally over-used. Daily protein intake should not exceed 1.2g per kg of body weight per day. Dosage for children is less than that for adults. See Nutritional Section of this Site Conclusion  Investigations, into people with persisting PCS, demonstrated that they applied more force over time to control balance. Helmich et al (2016, Med Sc Ex Sp, 48,  12, 2362-2368) proposed that in regard to cognitive processes, the increase of cerebral activation indicates an increase of attention demanding processes during postural control in altered environments. This is relevant in so far as individuals with post concussive symptomatology have a variety of symptoms including headache, dizziness, and cognitive difficulties that usually resolve over a few days to weeks. However, a subgroup of patients can have persistent symptoms which last months and even years. Complications in differential diagnosis, can arise clinically, when neck dysfunction and altered motor control occur concurrently due to both neck and cerebral pathology. For example, Whiplash and other traumatic head and neck injuries can result in pathology to both regions, whereas, more discreet altered cognitive processing from concussion can result in altered neck motor control. Musculoskelatal Physiotherapy can play a vital part in the treatment of neck dysfunction including the re-establishment of occulomotor proprioception and managing localized strength and cardiovascular exercise regimes. A total body, multi-disciplinary approach which is well co-ordinated amongst practitioners is vital to an optimal outcome.    Uploaded : 17 November 2017 Read More
  • Thu 24 Aug 2017

    Pain in the Brain - neural plasticity

    Pain in the Brain and Neural Plasticity by Martin Krause There are several mechanisms that can create a sensation of pain, which has been described as 'an unpleasent sensory and emotional experience in response to perceived or potential tissue damage'. Pain can be the result of peripheral sensitisation from peripheral inflammation, vascular compromise, necrosis, swelling, etc. Importantly, higher centres of the central nervous system not only perceive such sensitization of the peripheral nerve receptors, they can also modulate and control the intensity and tolerability of the perceived sensation through descending modulation at the peripheral receptor and in the spinal cord and through transcortical mechanisms depending on the 'meaning' and 'context given to the pain. Moreoever, the higher centres can create a 'state' of perceived 'threat' to the body through emotions such as fear and anxiety. Rather than the brain acting as a filter of unwanted sensation, in the higher centre induced pain state, rumination and magnification of sensations occur to create a pathological state.  Paradoxically, representation of body parts such as limbs and individual muscles can reduce in perceived size. In such instances the pain doesn't represent the sensation of pathology but rather pain has become the pathology. Hence, the brain generates pain in the brain, where the pain is perceived to be some sort of non-existant inflammatory or pathological sensation in the periphery. Evidence for this neural plasticity comes from imaging studies, where brain white matter structural properties have been shown to predict transition to chronic pain (Mansour et al 2013, Pain, 154, 10, 2160-2168). Specifically, differential structural connectivity to medial vs lateral prefrontal cortex and connectivity between medial prefrontal cortex and nucleus accumbens has been shown in people with persistent low back pain. In this case the back pain becomes the inciting event and given the persons' structural propensity, establishes specific functional coonectivity strength.  further reading Peripheral input is a powerful driver to neuroplasticity. Information gathered by touch, movement and vision, in the context of pain can lead to mal-adaptive plasticity, including the reorganisation of the somatosensory, and motor cortices, altered cortical excitability and central sensitisation. Examples of somatosensory reorganisation come from the work of Abrahao Baptista when investigating chronic anterior knee pain, who not only demonstrated reduced volume of Vastus Medialis but also is cortical translocation to another part of the cortex. ndividuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036, https://doi.org/10.1093/pm/pnx036)   AKP = anterior knee pain The same researcher (Abrahao Baptista) has shown that maximal tolerable electrical stimulation (eg TENS) of muscles can induce normalisation of the cortical changes through a process called 'smudging'. Transcortical stumilation has also been applied as a cortical 'primer' prior to the application of more traditional therapy such as motor re-training, exercise, and manipulation. Body illusions are another novel way to promote the normalisation of cortical function through adaptive neuroplasticity. Examples come from people with hand athritis, whose perception of their hand size is underestimated (Gilpin et al 2015 Rheumatology, 54, 4, 678-682). Using a curved mirror, similar to that in theme parks, the visual input can be increased to perceive the body part as larger (Preston et al 2011 DOI: 10.1093/rheumatology/ker104 · Source:PubMed ) . Irrespective of size, watching a reflection of the hand while performing synchronised movements enhances the embodiment of the reflection of the hand (Whitkopf et al 2017, Exp Brain res, 23, 5, 1933-1944). These visual inputs are thought to affect the altered functional connectivity between areas of the brain thereby affecting the 'pain matrix'. Another, novel way of looking at movement and pain perception is the concept of the motor engram. This has been defined as motor skill acquisition through the modification and organisation of muscle synergies into effective movement sequences. The learning process is thought to be acquired as a child through experientially based play activity. The specific neural mechanisms involved are unknown, however they are thought to include motor map topography reflecting the capacity for skilled movement reorganisation of motor maps in a manner that reflects the kinematics of aquired skilled movement map plasticity is supported by a reorganisation of cortical microcircuitry involving changes in synaptic efficacy motor map integrity and topography are influenced by various neurochemical signals that coordinate changes in cortical circuitry to encode motor experience (Monfils 2005 Neuroscientist, 11, 5, 471-483). Interestingly, it is an intriguing notion that accessing motor engrams from patterns aquired prior to the pain experience might lead a normalisation of brain activity. My personal experience of severe sciatica with leg pain, sleepness nights and a SLR of less than 30 degrees, happened to coincide with training my 9 year old sons soccer training. I was noticing that the nights after i trained the children, I slept much better and my range of movement improved. I commenced a daily program of soccer ball tricks which i had been showing the kids, including 'juggling', 'rainbows' and 'around the worlds'. Eventually, I even took up playing soccer again after a 30 year abscence from the sport. Other than new activity related pain issues (DOMS), four years on, the sciatica hasn't returned. I can only conclude that this activity activated dormant childhood motor engram, worked on global balance, mobilised my nerve, encouraged cross cortical activity and turned my focus into finctional improvement. Further explainations for my expereience comes from evidence suggesting that a peripheral adaptive pain state is initiated, whereby transcortical inhibiton occurs by the contralaleral hemisphere to the one which controls the affected limb. Additionally, excitation cortical (M1) drive of the muscles of the contralateral limb to the one which is in pain also occurs. In such cases re-establishement of motor drive to the affected side is important. In terms of tendon rehabilitation, external audtory and visual cues using a metronome have been employed and are showing promising results (Ebonie Rio et al 2017 Personal communication). In terms of my experience with the soccer ball tricks, the external visual cues and the cross talk from using left and right feet, head, shoulders, and chest during ball juggling manouvers, whilst calling the rhythm to the kids may have been the crucial factor to overcome the dysfunctional brain induced pain - muscle inco-ordination cycle, which I was in. Additionally, I was cycling which allowed me to focus on motor drive into the affected.limb. However, work by Lorrimer Moseley on CRPS has established that 'brain laterality' must be established before commencing trans-cortical rehabilitation techniques. Lorrimer's clinical interventions use 'mirror imaging' techniques which are only effective once the patient is able to discriminate the left and right sides of the affected body parts, presented visually, in various twists and angles.   Alternatively, the altered pain state can result in a hostage like situation, whereby the pain takes control. Similar to the 'Stockholm Syndrome' where the hostage begins to sympathise with their captors, so do some peoples brain states, where it begin to sympathise with the pain, creating an intractable bondage and dysfunctional state. One screening question which may reflect commitment to the process of rehabilitatation is to question whether they were able to resist the cookie jar when they were a child? Or were they committed to any sporting endeavours as a child? This may give some indication for the presence of motor engrams which can be used to overcome dysfunctional pain induced muscle synergies (neurotags), but also indicate an ability to be self disciplined, as well as being able to reconcile and identify goal oriented objectives, in spite of the cognitive pain processes? Remember that neurons that fire together, wire together. Uploaded : 18 October 2017 Read More
  • Thu 03 Aug 2017

    Sickle Cell Trait and Acute Low Back Pain

    Researchers believe that lumbar paraspinal myonecrosis (LPSMN) may contribute to the uncommon paraspinal compartment syndrome and that sickle cell trait (SCT) may play a role. Sustained, intense exertion of these lumbar paraspinal muscles can acutely increase muscle size and compartment pressure and so decrease arterial perfusion pressure. This same exertion can evoke diverse metabolic forces that in concert can lead to sickling in SCT that can compromise perfusion in the microvasculature of working muscles. In this manner, they believe that SCT may represent an additional risk factor for LPSMN. Accordingly, they presented six cases of LPSMN in elite African American football players with SCT. See link below http://journals.lww.com/acsm-msse/Fulltext/2017/04000/Acute_Lumbar_Paraspinal_Myonecrosis_in_Football.1.aspx Read More
  • Thu 03 Aug 2017

    Ibuprofen, Resistance Training, Bone Density

    Taking Ibuprofen immediately after resistance training has a deleterious effect on bone mineral content at the distal radius, whereas taking Ibuprofen or undertaking resistance training individually prevented bone mineral loss. http://journals.lww.com/acsm-msse/Fulltext/2017/04000/Effects_of_Ibuprofen_and_Resistance_Training_on.2.aspx Read More
  • Tue 11 Jul 2017

    Mitochondrial Health and Sarcopenia

    The aging process (AKA 30 years of age onwards), in the presence of high ROS (reactive oxygen species) and/or damaged mitochondrial DNA, can induce widespred mitochondrial dysfunction. In the healthy cell, mitophagy results in the removal of dysfunctional mitochondria and related material. In the abscence of functional removal of unwanted mitochondrial material, a retrograde and anterograde signalling process is potentially instigated, which results in both motor neuronal and muscle fibre apoptosis (death) (Alway, Mohamed, Myers 2017, Ex Sp Sc Rev, 45, 2, 58-69). This process is irreversible. Investigations in healthy populations, have shown that regular exercise improves the ability to cope with regular oxidative stress by the buffering and 'mopping up' of ROS agents which are induced as a result of exercise. It is plausible and highly probable that regular exercise throughout life can mitigate against muscle fibre death (Sarcopenia). Importantly, this process of muscle fibre death can commence in the 4th decade of life. and be as much as 1% per year. Reduction of muscle mass can result in immune and metabolic compromise, including subclinical inflammation, type II diabetes as well as the obvious reduction in functional capacity for activities of daily living. Published 11 July 2017 Read More
  • Thu 22 Dec 2016

    Ehlers Danlos Syndrome

    Is your child suffering Ehlers Danlos Syndrome? Hypermobile joints, frequent bruising, recurrent sprains and pains? Although a difficult manifestation to treat, physiotherapy can help. Joint Hypermobility Syndrome (JHS) by Martin Krause When joint hypermobility coexists with arthralgias in >4 joints or other signs of connective tissue disorder (CTD), it is termed Joint Hypermobility Syndrome (JHS). This includes conditions such as Marfan's Syndrome and Ehlers-Danlos Syndrome and Osteogenesis imperfecta. These people are thought to have a higher proportion of type III to type I collagen, where type I collagen exhibits highly organised fibres resulting in high tensile strength, whereas type III collagen fibres are much more extensible, disorganised and occurring primarily in organs such as the gut, skin and blood vessels. The predominant presenting complaint is widespread pain lasting from a day to decades. Additional symptoms associated with joints, such as stiffness, 'feeling like a 90 year old', clicking, clunking, popping, subluxations, dislocations, instability, feeling that the joints are vulnerable, as well as symptoms affecting other tissue such as paraesthesia, tiredness, faintness, feeling unwell and suffering flu-like symptoms. Autonomic nervous system dysfunction in the form of 'dysautonomia' frequently occur. Broad paper like scars appear in the skin where wounds have healed. Other extra-articular manifestations include ocular ptosis, varicose veins, Raynauds phenomenon, neuropathies, tarsal and carpal tunnel syndrome, alterations in neuromuscular reflex action, development motor co-ordination delay (DCD), fibromyalgia, low bone density, anxiety and panic states and depression. Age, sex and gender play a role in presentaton as it appears more common in African and Asian females with a prevalence rate of between 5% and 25% . Despite this relatively high prevalence, JHS continues to be under-recognised, poorly understood and inadequately managed (Simmonds & Kerr, Manual Therapy, 2007, 12, 298-309). In my clinical experience, these people tend to move fast, rely on inertia for stability, have long muscles creating large degrees of freedom and potential kinetic energy, resembling ballistic 'floppies', and are either highly co-ordinated or clumsy. Stabilisation strategies consist of fast movements using large muscle groups. They tend to activities such as swimming, yoga, gymnastics, sprinting, strikers at soccer. Treatment has consisted of soft tissue techniques similar to those used in fibromyalgia, including but not limited to, dry needling, myofascial release and trigger point massage, kinesiotape, strapping for stability in sporting endeavours, pressure garment use such as SKINS, BSc, 2XU, venous stockings. Effectiveness of massage has been shown to be usefull in people suffering from chronic fatigue syndrome (Njjs et al 2006, Man Ther, 11, 187-91), a condition displaying several clinical similarities to people suffering from EDS-HT. Specific exercise regimes more attuned to co-ordination and stability (proprioception) than to excessive non-stabilising stretching. A multi-modal approach including muscle energy techniques, dry needling, mobilisations with movement (Mulligans), thoracic ring relocations (especially good with autonomic symptoms), hydrotherapy, herbal supplementaion such as Devils Claw, Cats Claw, Curcumin and Green Tee can all be useful in the management of this condition. Additionally, Arnica cream can also be used for bruising. Encouragment of non-weight bearing endurance activities such as swimming, and cycling to stimulate the endurance red muscle fibres over the ballistic white muscles fibres, since the latter are preferably used in this movement population. End of range movements are either avoided or done with care where stability is emphasized over mobility. People frequently complain of subluxation and dislocating knee caps and shoulders whilst undertaking a spectrum of activities from sleeping to sporting endeavours. A good friend of mine, Brazilian Physiotherapist and Researcher, Dr Abrahao Baptista, has used muscle electrical stimulation on knees and shoulders to retrain the brain to enhance muscular cortical representation which reduce the incidence of subluxations and dislocations. Abrahao wrote : "my daughter has a mild EDS III and used to dislocate her shoulder many times during sleeping.  I tried many alternatives with her, including strenghtening exercises and education to prevent bad postures before sleeping (e.g. positioning her arm over her head).  What we found to really help her was electrostimulation of the supraspinatus and posterior deltoid.  I followed the ideas of some works from Michael Ridding and others (Clinical Neurophysiology, 112, 1461-1469, 2001; Exp Brain Research, 143, 342-349 ,2002), which show that 30Hz electrostim, provoking mild muscle contractions for 45' leads to increased excitability of the muscle representation in the brain (at the primary motor cortex).  Stimulation of the supraspinatus and deltoid is an old technique to hemiplegic painful shoulder, but used with a little different parameters.  Previous studies showed that this type of stimulation increases brain excitability for 3 days, and so we used two times a week, for two weeks.  After that, her discolcations improved a lot.  It is important to note that, during stimulation, you have to clearly see the humerus head going up to the glenoid fossa" Surgery : The effect of surgical intervention has been shown to be favourable in only a limited percentage of patients (33.9% Rombaut et al 2011, Arch Phys Med Rehab, 92, 1106-1112). Three basic problems arise. First, tissues are less robust; Second, blood vessel fragility can cause technical problems in wound closure; Third, healing is often delayed and may remain incomplete.  Voluntary Posterior Shoulder Subluxation : Clinical Presentation A 27 year old male presented with a history of posterior shoulder weakness, characterised by severe fatigue and heaviness when 'working out' at the gym. His usual routine was one which involved sets of 15 repetitions, hence endurance oriented rather than power oriented. He described major problems when trying to execute bench presses and Japanese style push ups.  https://youtu.be/4rj-4TWogFU In a comprehensive review of 300 articles on shoulder instability, Heller et al. (Heller, K. D., J. Forst, R. Forst, and B. Cohen. Posterior dislocation of the shoulder: recommendations for a classification. Arch. Orthop. Trauma Surg. 113:228-231, 1994) concluded that posterior dislocation constitutes only 2.1% of all shoulder dislocations. The differential diagnosis in patients with posterior instability of the shoulder includes traumatic posterior instability, atraumatic posterior instability, voluntary posterior instability, and posterior instability associated with multidirectional instability. Laxity testing was performed with a posterior draw sign. The laxity was graded with a modified Hawkins scale : grade I, humeral head displacement that locks out beyond the glenoid rim; grade II, humeral displacement that is over the glenoid rim but is easily reducable; and grade III, humeral head displacement that locks out beyond the glenoid rim. This client had grade III laxity in both shoulders. A sulcus sign test was performed on both shoulders and graded to commonly accepted grading scales: grade I, a depression <1cm: grade 2, between 1.5 and 2cm; and grade 3, a depression > 2cm. The client had a grade 3 sulcus sign bilaterally regardless if the arm was in neutral or external rotation. The client met the criteria of Carter and Wilkinson for generalized liagmentous laxity by exhibiting hyperextension of both elbows > 10o, genu recurvatum of both knees > 19o, and the ability to touch his thumbto his forearm Headaches Jacome (1999, Cephalagia, 19, 791-796) reported that migraine headaches occured in 11/18 patients with EDS. Hakim et al (2004, Rheumatology, 43, 1194-1195) found 40% of 170 patients with EDS-HT/JHS had previously been diagnosed with migraine compared with 20% of the control population. in addition, the frequency of migraine attacks was 1.7 times increased and the headache related disability was 3.0 times greater in migraineurs with EDS-HT/JHS as compared to controls with migraine (Bendick et al 2011, Cephalgia, 31, 603-613). People suffering from soft tissue hypermobility, connective tissue disorder, Marfans Syndrome, and Ehler Danlos syndrome may be predisposed to upper cervical spine instability. Dural laxity, vascular irregularities and ligamentous laxity with or without Arnold Chiari Malformations may be accompanied by symptoms of intracranial hypotension, POTS (postural orthostatic tachycardia syndrome), dysautonomia, suboccipital "Coat Hanger" headaches (Martin & Neilson 2014 Headaches, September, 1403-1411). Scoliosis and spondylolisthesis occurs in 63% and 6-15% of patients with Marfans syndrome repsectively (Sponseller et al 1995, JBJS Am, 77, 867-876). These manifestations need to be borne in mind as not all upper cervical spine instabilities are the result of trauma. Clinically, serious neurological complications can arise in the presence of upper cervical spine instability, including a stroke or even death. Additionally, vertebral artery and even carotid artery dissections have been reported during and after chiropractic manipulation. Added caution may be needed after Whiplash type injuries. The clinician needs to be aware of this possibility in the presence of these symptoms, assess upper cervical joint hypermobility with manual therapy techniques and treat appropriately, including exercises to improve the control of musculature around the cervical and thoracic spine. Atlantoaxial instability can be diagnosed by flexion/extension X-rays or MRI's, but is best evaluated by using rotational 3D CT scanning. Surgical intervention is sometimes necessary. An interesting case of EDS and it's affect on post concussion syndrome can be read elsewhere on this site. Temperomandibular Joint (TMJ) Disorders The prevelence of TMJ disorders have been reported to be as high as 80% in people with JHD (Kavucu et al 2006, Rheum Int., 26, 257-260). Joint clicking of the TMJ was 1.7 times more likely in JHD than in controls (Hirsch et al 2008, Eur J Oral Sci, 116, 525-539). Headaches associated with TMJ disorders tend to be in the temporal/masseter (side of head) region. TMJ issues increase in prevelence in the presence of both migraine and chronic daily headache (Goncalves et al 2011, Clin J Pain, 27, 611-615). I've treated a colleague who spontaneously dislocated her jaw whilst yawning at work one morning. stressful for me and her! Generally, people with JHD have increased jaw opening (>40mm from upper to lower incisors). Updated 17 October 2017  Read More
  • Fri 09 Dec 2016

    Physiotherapy with Sharna Hinchliff

    Physiotherapy with Sharna Hinchliff    Martin is pleased to welcome the very experienced physiotherapist Sharna Hinchliff to Back in Business Physiotherapy for one on one physiotherapy sessions with clients in 2017.  Sharna is a passionate triathelete and mother and has had several years experience working locally and internationally (New York and London) in the field of physiotherapy. Originally from Western Australia, Sharna graduated from the world renowned Masters of Manipulative Physiotherapy at Curtin University. read more Read More

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Updated : 10 May 2014

No responsibility is assumed by Back in Business Physiotherapy for any injury and/or damage to persons or property as a matter of product liability, negligence, or from any use of any methods, products, instruction, or ideas contained in the material in this and it's related websites. Because of rapid advances in the medical sciences, the author recommends that there should be independent verification of diagnoses and exercise prescription. The information provided on Back in Business Physiotherapy is designed to support, not replace, the relationship that exists between a patient/site visitor and their treating health professional.

Copyright Martin Krause 1999 - material is presented as a free educational resource however all intellectual property rights should be acknowledged and respected