Category Archives: Neurotrauma

¿Es realmente preocupante la hemorragia subaracnoidea traumática?

In 661 patients with isolated tSAH. Only four patients (0.61%) underwent any sort of aggressive neurosurgical, medical, or endovascular intervention, regardless of GCS score. Most tSAH patients without additional systemic injury were discharged home (68%), including 53% of patients with a GCS score of 3-8. However, older patients were more likely to be discharged to a rehabilitation facility (p<0.01). There were six (1.7%) in-hospital deaths, and five patients of these patients were older than 80 years old. Isolated tSAH, regardless of admission GCS score, is a less severe intracranial injury that is highly unlikely to require aggressive operative, medical, or endovascular intervention, and is unlikely to be associated with major neurologic morbidity or mortality, except perhaps in elderly patients. Based upon our findings, we argue that impaired consciousness in the setting of isolated tSAH should strongly compel a consideration of non-traumatic factors in the etiology of the altered neurological status1

  1. Lee JJ, Segar DJ, Asaad WF. Comprehensive Assessment of Isolated Traumatic Subarachnoid Hemorrhage. J Neurotrauma. 2014 Feb 6. [Epub ahead of print] PubMed PMID: 24224706. []

Coagulometría rápida para pacientes urgentes

Con el creciente uso de la anticoagulación oral mediante antagonistas de la vitamina K,  los neurocirujanos se encuentran con un número creciente de pacientes que requieren una rápida reversión de los efectos anticoagulantes, para realizar procedimientos quirúrgicos urgentes.

La iniciación de estos procedimientos se retrasa debido a que el estado de coagulación debe ser evaluada a través del examen de muestras de sangre en los laboratorios centrales.

Este retraso puede dar lugar a efectos negativos, sobre todo en situaciones que potencialmente amenazan la vida tales como la hemorragia intracraneal.

Los dispositivos de punto de atención para la evaluación del índice internacional normalizado (INR POC) han mejorado el manejo de la anticoagulación en el ámbito ambulatorio.

El uso de estos dispositivos puede también tener efectos beneficiosos en el tratamiento de pacientes anticoagulados que precisan procedimientos neuroquirúrgicos urgentes.

El  coagulómetro CoaguChek XS (®) fue utilizado en 17 pacientes con antecedentes de uso de anticoagulantes y una condición que requiere reversión de la anticoagulación urgente antes de un procedimiento neuroquirúrgico (trepanación: n = 8, craneotomía: n = 7, laminectomía: n = 2).

No hubo dificultades técnicas, y se logró una evaluación rápida del INR en todos los casos en 2 min. Los valores de INR POC tenían buena correlación con la evaluación del laboratorio central. Con una desviación media del INR 0.036 ± 0.12.

La ganancia media de tiempo a través del uso del dispositivo de INR POC en comparación con la evaluación del laboratorio central fue de 47 ± 6 min (intervalo: 37-61 min).

Las experiencias iniciales con un dispositivo de estas características en pacientes anticoagulados que precisan procedimientos neuroquirúrgicos urgentes demuestran que su uso puede contribuir a una mejor gestión de estos pacientes1.

  1. Beynon C, Jakobs M, Rizos T, Unterberg AW, Sakowitz OW. Rapid bedside coagulometry prior to urgent neurosurgical procedures in anticoagulated patients. Br J Neurosurg. 2014 Jan;28(1):29-33. doi: 10.3109/02688697.2013.869549. Epub 2013 Dec 9. PubMed PMID: 24313307. []

Secuencia de imagen potenciada en susceptibilidad paramagnética (SWI) en el traumatismo craneoencefálico

Es capaz de detectar pequeñas hipointensidades como signo de daño crónico y agudo en la conmoción cerebral.

Las alteraciones sugieren una disminución del espacio extracelular, y la disminución de difusividad en la sustancia blanca.

Este hallazgo podría explicarse por el edema y/o por el aumento de células gliales.

A pesar de estos resultados no se ha podido determinar si las alteraciones microestructurales observadas están relacionadas con la patología a largo plazo o por persistencia de los síntomas.

Sin embargo, establece un panorama más claro de cómo el cerebro responde a la conmoción cerebral12

  1. Helmer KG, Pasternak O, Fredman E, Preciado RI, Koerte IK, Sasaki T, Mayinger M, Johnson AM, Holmes JD, Forwell LA, Skopelja EN, Shenton ME, Echlin PS. Hockey Concussion Education Project, Part 1. Susceptibility-weighted imaging study in male and female ice hockey players over a single season. J Neurosurg. 2014 Feb 4.[Epub ahead of print] PubMed PMID: 24490839. []
  2. Pasternak O, Koerte IK, Bouix S, Fredman E, Sasaki T, Mayinger M, Helmer KG, Johnson AM, Holmes JD, Forwell LA, Skopelja EN, Shenton ME, Echlin PS. Hockey Concussion Education Project, Part 2. Microstructural white matter alterations in acutely concussed ice hockey players: a longitudinal free-water MRI study. J Neurosurg. 2014 Feb 4. [Epub ahead of print] PubMed PMID: 24490785. []

Update: Chronic subdural hematoma and anticoagulant therapy

Chronic subdural hematoma and anticoagulant therapy

J.Sales-Llopis

Neurosurgery Department, University General Hospital of Alicante, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Alicante, Spain

Chronic subdural hematoma (CSDH) in the elderly population, especially in men, is frequently associated with falls and anticoagulation or antithrombotic therapy. The indication for these medications, especially in elderly patients at risk for falls, should be carefully evaluated and controlled 1).

This association, for patients under anticoagulant therapy, appears even stronger in those patients who develop a CSDH in the absence of a recent trauma 2)

The risk of developing a CSDH was at least 42.5 times higher in warfarinised patients and also increased for patients on aspirin, although this risk could not be quantified 3).

A patient undergoing aspirin treatment must be considered at risk of development of chronic subdural hematoma. Aspirin should not be prescribed to patients with post-traumatic headaches 4).

Bilateral hematoma

The bilateral hematomas tended to happen in hemodialysis cases, and in patients on warfarin or anti-platelet drugs. Bilateral hematomas were found in 41.7%, 37.5% and 33.3% respectively. The ratio of PT and aPTT coagulation time was as follows: PT ratio was 1.040 in hemodialysis cases and 1.082 in warfarin-applicated cases. aPTT ratio was 1.022 in hemodialysis cases and 1.055 in warfarin-applicated cases. These results suggest that the suppressed coagulation ability and platelet function are involved in the genesis of bilateral chronic subdural hematomas 5).

Restarting

Clinicians regularly confront the dilemma of whether or not to restart anticoagulant and antiplatelet medication after CSDH, yet there is little evidence to support the decision-making process.

Databases including MEDLINE, Cochrane, ISI Web of Knowledge, Embase and Google Scholar were searched for retrospective and prospective studies looking specifically at patients presenting with CSDH whilst on anticoagulant or antiplatelet medication which had data on subsequent recurrence and thromboembolic events.

Three relevant studies were found, totalling to 64 patients. In those restarted on anticoagulation, 11.1% experienced recurrences and 2.2% experienced thromboembolic events. In the control group that was not restarted on anticoagulation, 22.2% experienced recurrences and no patient experienced thromboembolic events. All recurrences and thromboembolic events occurred within the first 4 weeks of the initial surgical evacuation. Conclusions. The review seems to paradoxically suggest a lower bleeding risk and a higher thromboembolism risk when anticoagulation is restarted, although few concrete conclusions can be drawn from a pool of 64 patients. The decision on whether or not to restart anticoagulation in patients who present with CSDH whilst on anticoagulation has little empirical evidence to support a decision either way; more data are required to allow clinicians to make informed decisions about whether or not to restart anticoagulation, and if so, which drug, at what time-point and at what dose/therapeutic target 6).

Gonugunta et al. suggest recommencing warfarin 3 weeks after surgical evacuation of CSDH in anticoagulated patients 7).

Early resumption of anticoagulant therapy (within 3 days) did not cause intracranial rebleeding in any operative patient. All the chronic SDH patients and some of the subcortical hematoma patients had a good outcome 8).

For Yeon et al. restarting warfarin therapy does not need to be withheld for more than 3 days after burr hole drainage, particularly in patients with a high thromboembolic risk 9).

Case series

2013

A retrospective review of 239 patients undergoing surgery for CSDH over a period of six years (2006-2011). The majority of patients (63%) in the non-trauma group were receiving anticoagulants and/or antiplatelet agent therapy prior to CSDH presentation, compared to 42% in the trauma group. Twenty-four percent experienced recurrence of the CSDH. There was no association between recurrence and anticoagulant and/or antiplatelet agent therapy.

Anticoagulant and/or antiplatelet aggregation agent therapy is more prevalent among non-traumatic CSDH patients but does not seem to influence the rate of CSDH recurrence 10).

2009

In the non-trauma group 71% of patients were treated with anticoagulants or antiplatelet aggregation agents (AAA) compared to 18% in the trauma group. Considering only AAA, 59% of the non-trauma patients were treated with these drugs versus 17% of patients in the trauma group. The recurrence rate for all patients was 17%. These findings confirm that the use of anticoagulants and AAA is over-represented in patients with non-traumatic CSDH. In this study, recurrence was not associated with previous use of anticoagulants or AAA 11).

2006

Eighty-one cases of chronic subdural haematomas (CSDH) admitted to the neurosurgical unit of the Royal Hobart Hospital, Tasmania, Australia, over a 5-year period were reviewed. The use of anticoagulant therapy as a causative agent in the development of CSDH was investigated. We suspected a high incidence of anticoagulant or anti-thrombotic therapy. We found that anticoagulant therapy was used by a significant percentage of CSDH patients. In the patient group presenting to our unit the risk of developing a CSDH was at least 42.5 times higher in warfarinised patients and also increased for patients on aspirin, although this risk could not be quantified 12).

2001

There is a perception that patients who develop a chronic subdural haematoma (CSDH), whilst taking warfarin, do less well than those not taking warfarin. This study looks at such patients to determine the truth of this perception. A retrospective analysis of two time periods (1990-1992 and 1995-1997) looking at all patients with CSDH admitted to this neurosurgical unit for treatment, to determine the incidence and to look more closely at those on warfarin. The influence of warfarin on the incidence, severity and outcome has been studied. Between 1990 and 1992, 11.8% of those patients with CSDH were taking warfarin, whilst in 1995-1997 20% were on warfarin. The overall number of referrals of CSDH increased from 34 to 150 patients during these time periods. There were no differences in age, sex or other medical disorders between the two groups. No adverse events occurred when the warfarin was stopped temporarily for treatment of the CSDH. There was no increase in recurrence rate in those on warfarin, compared with those not on warfarin. This study, whilst demonstrating an increase in the number of referrals of CSDH and patients with CSDH taking warfarin, has not demonstrated an adverse effect of the warfarin on the outcome of treatment for CSDH. The authors suggest recommencing warfarin 3 weeks after surgical evacuation of CSDH in anti coagulated patients 13).

1999

The records of seven patients with mean GCS = 14.2 and mean clinical grade = 1.85 affected by chronic subdural hematoma and in treatment with anticoagulants were examined retrospectively. All the patients underwent subtemporal craniectomy plus closed drainage or burrhole(s) plus closed drainage after immediate correction of hypocoagulability by administration of vitamin K and fresh frozen plasma and normalization of PA by calcium heparin.

Outcome was good for all the patients except one who died because of cerebral herniation due to massive solid subdural hematoma during extracorporeal dialysis. Complications included: intracerebral hemorrhage, solid subdural hematoma, slow brain reexpansion, subdural collection reaccumulation and cerebral embolism. Three patients required re-operation. Mean duration of hospital stay was 18 days with range from 7 to 24 days.

Basing on this retrospective study and the proposed pathophysiology, the guidelines for optimal management of this subgroup of patients are proposed. Recommendations include the immediate correction of hypocoagulability, the appropriate surgical technique and the cautious conversion to oral anticoagulation as well as the appropriate timing of such conversion 14).

1995

In 2 patients, warfarin was discontinued and its effect neutralized by vitamin K, then surgery was performed after the thrombotest value exceeded 50%. No uncontrollable bleeding occurred at surgery. Warfarin was discontinued until 3-7 days postoperatively. Intravenous heparin administration was used to prevent embolic complications and the dose was modified based on the activated clotting time measured at the bedside. One patient, who could not receive heparin administration because of massive bleeding, developed myocardial infarction due to coronary artery thromboembolism 2 days after operation and died 4 days later. The other patients received heparin administration and were alive and well at the most recent follow-up examinations. Heparin administration monitored by activated clotting time is a useful method to prevent embolic and bleeding complications in the surgical treatment of intracranial hemorrhage in patients with prosthetic heart valves receiving long-term anticoagulant therapy15).

1991

3 cases with good outcome They recommend conservative treatment is to be the first choice, if conditions allow it. Surgery can be performed by burr hole irrigation when indicated. Precautions should be taken not to injure the inner membrane of the hematoma or the brain proper, and the need for slow decompression should be kept in mind 16).

Case reports

2014

A 78-year-old man who had a history of myocardial and cerebral infarction and who was treated with aspirin and warfarin, presented with left chronic subdural hematoma. Cerebral computed tomography showed severe brain compression of hematoma with midline shift, indicating the need for emergent surgery. The hematology and clotting tests upon admission revealed severe thrombocytopenia (platelet count, 1.3 × 10(4)/μL) with normal clotting activity. Because platelet aggregation was evident in the smear, we re-examined the patient for hematology using tubes that contained heparin, showing also low platelet count (2.3 × 10(4)/μL). The day on admission, we performed irrigation and drainage of the chronic subdural hematoma through single burr-hole craniostomy. During surgery, we used 10 units of platelet concentrates (PCs) for the reason that the patient was taking aspirin and coagulopathy derived from low platelet count could not be excluded. After surgery, we re-evaluated the hematology of the blood stored in tubes that contained ethylenediaminetetraacetic acid (EDTA) with or without kanamycin (KM). Treatment with KM dissociated EDTA-induced platelet aggregation and revealed platelet counts with highest accuracy (no KM treatment, 1.3 × 10(4)/μL; KM treatment, 15.2 × 10(4)/μL). This phenomenon is called EDTA-Dependent Pseudothrombocytopenia (PTCP) defined as falsely low platelet counts reported by automated hematology analyzers due to platelet aggretgation. Awareness of the phenomenon will enable neurosurgeons to manage patients with PTCP appropriately and clinical laboratory especially in emergency hospital is recommended to prepare for the hematological tubes being added KM in routine analysis, resulting in preventing mistaken diagnosis 17).

2010

A 64-year-old female receiving clopidogrel and aspirin antiaggregation therapy after percutaneous coronary intervention for non-STEMI myocardial infarction developed nontraumatic bilateral subdural hematoma with dizziness, vertigo and headache. Craniotomy had to be postponed because of reduced ADP platelet aggregability. Four days after clopidogrel withdrawal and transfusion of 12 platelet concentrate units, ADP aggregation transiently normalized and bilateral trepanation with hematoma evacuation was performed. The procedure was followed by excellent neurologic and clinical recovery; however, decreased platelet aggregability was recorded by postoperative day 12 despite strict clopidogrel and other platelet inhibitor withdrawal. Suspicion of Glanzmann thrombastenia was excluded by flow cytometry. Two weeks after neurosurgery, the right femoral vein thrombosis was detected by color doppler ultrasonography and therapy with fractionated heparin was initiated, followed by warfarin. The risk and incidence of hemorrhagic complications of antiaggregation and anticoagulation therapy are discussed. Caution is warranted on prescribing this potentially harmful therapy to older patients, generally burdened with other chronic comorbidities 18).

2003

We present a patient on warfarin in whom a drainage port system was attached to the skull, successfully draining a subacute subdural hematoma.

An elderly male presented to our institution with right hemiparesis a week following a motor vehicle accident. He was on warfarin for recurrent pulmonary emboli and suffered from severe coronary artery disease. Physical examination demonstrated a grade 3/5 hemiparesis and a computerized tomography (CT) scan confirmed the diagnosis of subacute subdural hematoma. He underwent twist drill craniostomy and attachment of the subdural evacuating port system. Recovery in this patient was dramatic.

The subdural evacuating port system (SEPS) permits the neurosurgeon to drain subacute or chronic hematomas by a method that is minimally invasive, simple, and safe. The SEPS appears to promote brain expansion without the potential biohazards of other standard techniques 19).

1984

Nobuoka W, Konishi M, Asazuma S, Iwamoto T, Hamashima T. [A case of chronic subdural hematoma developing during long-term anticoagulant drug therapy after mitral valve replacement]. Rinsho Kyobu Geka. 1984 Sep;4(5):603-5. Japanese. PubMed PMID: 6522985 20)

References

1) Baechli H, Nordmann A, Bucher HC, Gratzl O. Demographics and prevalent risk factors of chronic subdural haematoma: results of a large single-center cohort study. Neurosurg Rev. 2004 Oct;27(4):263-6. Epub 2004 May 18. PubMed PMID: 15148652.
2) De Bonis P, Trevisi G, de Waure C, Sferrazza A, Volpe M, Pompucci A, Anile C, Mangiola A. Antiplatelet/anticoagulant agents and chronic subdural hematoma in the elderly. PLoS One. 2013 Jul 12;8(7):e68732. doi: 10.1371/journal.pone.0068732. Print 2013. PubMed PMID: 23874740; PubMed Central PMCID: PMC3709887.
3) , 12) Rust T, Kiemer N, Erasmus A. Chronic subdural haematomas and anticoagulation or anti-thrombotic therapy. J Clin Neurosci. 2006 Oct;13(8):823-7. PubMed PMID:16997707.
4) Reymond MA, Marbet G, Radü EW, Gratzl O. Aspirin as a risk factor for hemorrhage in patients with head injuries. Neurosurg Rev. 1992;15(1):21-5. PubMed PMID: 1584433.
5) Oyama H, Ikeda A, Inoue S, Shibuya M. [The relationship between coagulation time and bilateral occurrence in chronic subdural hematoma]. No To Shinkei. 1999 Apr;51(4):325-30. Japanese. PubMed PMID: 10363267.
6) Chari A, Clemente Morgado T, Rigamonti D. Recommencement of anticoagulation in chronic subdural haematoma: a systematic review and meta-analysis. Br J Neurosurg. 2014 Jan;28(1):2-7. doi: 10.3109/02688697.2013.812184. Epub 2013 Jul 8. Review. PubMed PMID: 23834661.
7) , 13) Gonugunta V, Buxton N. Warfarin and chronic subdural haematomas. Br J Neurosurg. 2001 Dec;15(6):514-7. PubMed PMID: 11814005.
8) Kawamata T, Takeshita M, Kubo O, Izawa M, Kagawa M, Takakura K. Management of intracranial hemorrhage associated with anticoagulant therapy. Surg Neurol. 1995 Nov;44(5):438-42; discussion 443. PubMed PMID: 8629228.
9) Yeon JY, Kong DS, Hong SC. Safety of early warfarin resumption following burr hole drainage for warfarin-associated subacute or chronic subdural hemorrhage. J Neurotrauma. 2012 May 1;29(7):1334-41. doi: 10.1089/neu.2011.2074. Epub 2012 Jan 2perative patient. All the chronic SDH patients and some of the subcortical hematoma patients had a good outcome ((Kawamata T, Takeshita M, Kubo O, Izawa M, Kagawa M, Takakura K. Management of intracranial hemorrhage associated with anticoagulant therapy. Surg Neurol. 1995 Nov;44(5):438-42; discussion 443. PubMed PMID: 8629228.
10) Aspegren OP, Åstrand R, Lundgren MI, Romner B. Anticoagulation therapy a risk factor for the development of chronic subdural hematoma. Clin Neurol Neurosurg. 2013 Jul;115(7):981-4. doi: 10.1016/j.clineuro.2012.10.008. Epub 2012 Nov 3. PubMed PMID: 23128014.
11) Lindvall P, Koskinen LO. Anticoagulants and antiplatelet agents and the risk of development and recurrence of chronic subdural haematomas. J Clin Neurosci. 2009 Oct;16(10):1287-90. doi: 10.1016/j.jocn.2009.01.001. Epub 2009 Jun 28. PubMed PMID: 19564115.
14) Zingale A, Chibbaro S, Florio A, Distefano G, Porcaro S. Management of chronic subdural hematoma in patients treated with anticoagulation. J Neurosurg Sci. 1999 Dec;43(4):277-84. PubMed PMID: 10864390.
15) Nakagawa T, Kubota T, Handa Y, Kawano H, Sato K. Intracranial hemorrhage due to long-term anticoagulant therapy in patients with prosthetic heart valves–four case reports. Neurol Med Chir (Tokyo). 1995 Mar;35(3):156-9. PubMed PMID: 7770109.
16) Kinjo T, Mukawa J, Nakata M, Kinjo N. [Chronic subdural hematoma secondary to coagulopathy]. No Shinkei Geka. 1991 Oct;19(10):991-7. Japanese. PubMed PMID: 1944787.
17) Tosa M, Fujita H, Ishihama Y, Nishimura S, Ide T. Chronic subdural hematoma in elderly patient with EDTA-dependent pseudothrombocytopenia recently treated with aspirin and warfarin: case report. Neurol Med Chir (Tokyo). 2014;54(5):401-4. Epub 2014 Jan 28. PubMed PMID: 24477063.
18) Vuk A, Stancić V, Rincić G, Ledinsky M, Grbac L, Stancić N. Nontraumatic bilateral subdural hematoma caused by antiaggregation therapy: case report and review of the literature. Acta Clin Croat. 2010 Jun;49(2):163-8. PubMed PMID: 21086734.
19) Asfora WT, Schwebach L. A modified technique to treat chronic and subacute subdural hematoma: technical note. Surg Neurol. 2003 Apr;59(4):329-32; discussion 332. PubMed PMID: 12748020.
20) Nobuoka W, Konishi M, Asazuma S, Iwamoto T, Hamashima T. [A case of chronic subdural hematoma developing during long-term anticoagulant drug therapy after mitral valve replacement]. Rinsho Kyobu Geka. 1984 Sep;4(5):603-5. Japanese. PubMed PMID: 6522985.

Brain Injury and Neuropsychological Rehabilitation: International Perspectives (Institute for Research in Behavioral Neuroscience Series)

Brain Injury and Neuropsychological Rehabilitation: International Perspectives (Institute for Research in Behavioral Neuroscience Series)

 

Product Description

Most individuals with brain damage experience a curtailment or loss of lifestyle without rehabilitation. Improved methods and appropriately timed medical interventions now make it possible for more individuals to survive brain insults and to be assisted by rehabilitation neuropsychologists in achieving renewed commitment to life. Damage to the brain — the organ of human emotions and cognition — reduces psychological functioning and realistic adaptation, and the patient and his/her family are often encapsulated in the time prior to injury. To regain part or most of the lifestyle lost, an honest, dedicated, and realistic approach is required. Neuropsychological rehabilitation can provide tools for this task, provided that the most comprehensive, elaborate and knowledge-based methods are integrated in the training, and provided that knowledge from many disciplines and from community environments and family is encompassed.

In the present book knowledge representing the development of neuropsychological rehabilitation during the past five years is collected from a conference titled “Progress in Neuropsychological Rehabilitation.” The chapters are written by professionals who were invited to share their experiences from different areas within the field because of their expertise with processes involved in neuropsychological rehabilitation. After a historical review, the chapters follow a visible sequence from biology to neuropsychology and neuropharmacology. Experts discuss the most advanced medical knowledge of the effect of injury on states of the organism. The second part of the book is dedicated to the outcome and the economics of rehabilitation as well as plans for the future. Finally, a panel discussion addresses the overall concept: Is rehabilitation worthwhile and ethical? The reactions — influenced by the cross-cultural exchange of knowledge — shed light on the essence and practice of today’s neurorehabilitation.


Product Details

  • Published on: 2014-01-02
  • Released on: 2014-01-02
  • Format: Kindle eBook

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¿De la escala Glasgow a la FOUR Score?

La escala de Glasgow para el coma ha sido adoptada de forma generalizada, a pesar de presentar importantes limitaciones,  entre las que destacan la imposibilidad de valorar la respuesta verbal en pacientes intubados o afásicos,  y la no valoración de los reflejos del tronco encefálico, que aportan importante información pronóstica.

Escala

Se compone de cuatro categorías clínicamente distintas de evaluación

Respuesta ocular

4. Dirige la mirada horizontal o verticalmente o parpadea dos veces cuando se le solicita

3. Abre los ojos espontáneamente, pero no dirige la mirada

2. Abre los ojos a estímulos sonoros intensos

1. Abre los ojos estímulos nociceptivos

0. Ojos cerrados, no los abre al dolor

Respuesta motora

4. Eleva los pulgares, cierra el puño o hace el signo de la victoria cuando se le pide

3. Localiza al dolor (aplicando un estímulo supraorbitario o temporomandibular)

2. Respuesta flexora al dolor (incluye respuestas en decorticación y retirada) en extremidad superior

1. Respuesta extensora al dolor

0. No respuesta al dolor, o estado mioclónico generalizado

Reflejos de tronco

4. Ambos reflejos corneales y fotomorores presentes

3. Reflejo fotomotor ausente unilateral

2. Reflejos corneales o fotomotores ausentes

1. Reflejos corneales y fotomotores ausentes

0. Reflejos corneales, fotomotores y tusígeno ausentes

Respiración

4. No intubado, respiración rítmica

3. No intubado, respiración de Cheyne-Stokes

2. No intubado, respiración irregular

1. Intubado, respira por encima de la frecuencia del respirador

0. Intubado, respira a la frecuencia del respirador o apnea

La puntuación total puede tomar por tanto valores entre 16 (consciente) y 0 puntos (coma arreactivo sin reflejos de tronco encefálico).

La escala FOUR ha sido validada por sus autores, con una buena concordancia entre observadores y una relación lineal con la mortalidad, permitiendo además distinguir distintos grados de afectación entre los pacientes con puntuaciones bajas en la escala de Glasgow 1).

Entre las ventajas teóricas de la escala FOUR se encuentran su capacidad para detectar el síndrome de enclaustramiento, así como distintos estadios de la herniación cerebral.

Se ha señalado que la escala FOUR sería insuficiente para detectar el estado vegetativo y los estados de mínima conciencia 2).

Resultados

Es una escala fiable para evaluar el nivel de conciencia en los pacientes con accidente cerebrovascular agudo, mostrando una buena correlación con la GCS y la escala de ictus del NIH 3)

Ha mostrado más robustez que la Glasgow Coma Scale (GCS) en la predicción de mortalidad a los 30 días en pacientes neuroquirúrgicos con conciencia severamente dañada. No hubo diferencias relevantes en la predicción pobre y buen resultado con respecto a las escala de Glasgow4).

1) Wijdicks EF, Bamlet WR, Maramattom BV, Manno EM, McClelland RL. Validation of a new coma scale: The FOUR score. Ann Neurol 2005; 58: 585-593.
2) Schnakers C, Giacino J, Kalmar K, Piret S, Lopez E, Boly M, Malone R, Laureys S. Does the FOUR score correctly diagnose the vegetative and minimally conscious states? Ann Neurol 2006; 60: 744-745; author reply 745
3) Idrovo L, Fuentes B, Medina J, Gabaldón L, Ruiz-Ares G, Abenza MJ, Aguilar-Amat MJ, Martínez-Sánchez P, Rodríguez L, Cazorla R, Martínez M, Tafur A, Wijdicks EF, Diez-Tejedor E. Validation of the FOUR Score (Spanish Version) in acute stroke: an interobserver variability study. Eur Neurol. 2010;63(6):364-9. doi: 10.1159/000292498. Epub 2010 Jun 16. PubMed PMID: 20551672.
4) Chen B, Grothe C, Schaller K. Validation of a new neurological score (FOUR Score) in the assessment of neurosurgical patients with severely impaired consciousness. Acta Neurochir (Wien). 2013 Nov;155(11):2133-9; discussion 2139. doi: 10.1007/s00701-013-1854-2. Epub 2013 Sep 8. PubMed PMID: 24013867.