The Post-Concussion Syndrome: A Diagnostic Analysis

There are over 1 million mild traumatic brain injuries (MTBI) in the United States today, accounting for 85% of all traumatic brain injuries (Bazarian et al, 2005)¹. MTBI injury was formerly referred to as concussion (Ruff et al, 2009)², a diffuse disorder of brain cells generated by traumatic shock, but short of discernible permanent structural injury. MTBI is the most common diagnosis for referral to a neuropsychologist due to personal injury (Ruff and Richardson, 1999; Sweet and Meyers, 2012)³. Researchers have had many years to study MTBI, enabling a clearer picture regarding definitional and research design problems (Larrabee, G, 2005)⁴.

Post-concussion syndrome – a mixed neurological/psychological disorder

This syndrome is one of several that stand on the border between neurological (organic) and psychological. It begins with a head injury from which the patient seemingly makes recovery but then continues as a psychological condition long after any visible indices of brain damage have resolved (Lishman, W A, 1973).⁵ He noted that post-concussion syndrome (PCS) represents the most frequent psychological sequelae of head injury by pointing out that the longer psychological symptoms persist, the less likely they are an expression of actual brain damage. And as Symonds said almost three-quarters of a century ago, “It is not only the kind of injury that matters but the kind of head.” (Symonds, C P, 1937)⁶.

Psychological reactions are an all-too-common consequence of PCS. Few physical injuries fail to be compounded by some additional degree of psychological response. Approximately one-third of all people requiring medical attention following an accident (and particularly the kinds of accidents likely to eventuate in litigation) are found to also suffer a significant adverse psychological response (O’Donnel, M L et al, 2004)⁷.

While a posttraumatic psychological reaction may occur in someone who previously had not the slightest psychological difficulty, it is far more likely in the emotionally-predisposed individuals, whose pre-trauma personality is characterised by such elements as compensatory drive, perfectionism, self-reliance, overachievement, and a preoccupation with control issues. (Fann and Sussex, 1976)⁸. For example, if the patient was to collapse psychologically following a modest concussion from which apparently good objective recovery was made, there were likely significant psychological problems prior to the concussion, the trauma merely providing a focal point around which such difficulties might coalesce and become manifestly symptomatic.

It is the patient’s preexisting disequilibrium that plays a far larger role than the actual concussion in creating neuropsychological symptoms that follow the index trauma, the event serving more as a vehicle for rendering previous emotional and psychological problems into physical form. The plaintiff’s attorney would argue most reasonably that the patient had some problems but no manifest symptoms prior to injury and such problems the patient possessed merely predisposed them to the disability which followed. It falls to the defence to demonstrate that an illness need not be visibly symptomatic to be present, just as a cancer may be present and even incurable long before the patient develops a palpable lump or persistent cough, and that the patient was not merely predisposed or vulnerable prior to injury, but psychologically impaired (i.e. psychological disequilibrium) long before the allegedly precipitant event.

When symptoms of a concussion persist beyond expectation they are frequently described as post-concussion syndrome (PCS; Gunstad and Suhr, 2004)⁹. Hence, PCS is defined as a form of physical, psychological and cognitive impairment characterised by memory and other cognitive deficits, headache, dizziness, fatigue, apathy, difficulty concentrating, personality change, emotional ability, irritability, depression and anxiety (Alexander, M P, 1995)¹⁰. Here, the patient’s predisposition as noted above is just as important as the traumatic impact, as different individuals will react in markedly disparate ways to what appears to be objectively the same degree of injury. Older people and people at a clinical juncture in life are particularly vulnerable. Socioeconomic status can also be a determinative factor: A janitor may continue to perform their duties acceptably despite a modest degree of brain injury that would retire a PhD. In short, what may matter is not only the degree of concussion, but the number of degrees the concussion patient holds.

To date, there are three conceptual positions of concussion, presently termed mild traumatic brain injury (MTBI). The first is that there is a relatively small percentage of MTBI patients that experience lasting problems for physical (i.e. neurological verifiable) reasons (Ruff, Iverson, Barth, Bush, & Broschek, 2009)¹¹. The second position is that the residual problems arising from MTBI are more psychological (i.e., medically unverifiable, non-neurological) (Uzzell, 1999)¹². The final position is that of Larrabee (1999) and Binder (1997)¹³ , who deny residual problems until further scientific investigations are conducted.

Hence, the purpose of this article is intended to provide attorneys with an updated perspective on the PCS diagnosis, and even consider its definitional dismissal from clinical and forensic use.

Traumatic brain injury consists of four categories of severity: mild, complicated-mild, moderate, and severe. MTBIs are defined by any alteration in mental status (e.g. feeling “dazed”), loss of consciousness of 30 minutes or less, post injury memory loss (posttraumatic amnesia) of 24 hours or less, and a Glasgow Coma Scale (GCS) score (an index of brain responsiveness) of 13 or higher. Complicated-mild traumatic brain injuries are MTBIs plus intracranial (i.e., inside the skull) bleeding, typically found in the emergency room brain CT or MRI. Moderate and Severe traumatic brain injuries require progressively more severe injury characteristics with intracranial bleeding and low GCS scores, 9-12 and 3-8 respectively.

There are many MTBI definitions, but the most widely used is from the American Congress of Rehabilitation Medicine (ACRM; Anderson-Barnes, Weeks, and Tsao, 2010)¹⁴ , making it useful in forensic cases. However, no mention is made in this definition about intracranial bleeding, which is the hallmark of a complicated-mild traumatic brain injury. Therefore, it is important to emphasise that any definition of MTBI should exclude bleeding inside the skull, thereby differentiating between MTBIs and complicated-mild traumatic brain injuries. At present, brain injury severity is not characterized this way i.e., all intracranial bleeding associated with MTBI is viewed equally. Since research is differentiating between MTBIs and complicated-mild traumatic brain injuries it is incumbent upon not only clinicians but also attorneys to make this distinction in their medical-legal cases.

The purpose of this article is intended to provide attorneys with an updated perspective on the PCS diagnosis, and even consider its definitional dismissal from clinical and forensic use.

The Problems With the Post-Concussion Syndrome Diagnosis

According to the International Classification of Diseases, 10^th Revision, Clinical Modification (ICD-10-CM; Goodheart, 2014)¹⁵; there is a diagnostic category called PCS. It is applied for those who succumb to a concussion followed by the triage of physical, psychological and cognitive symptoms that extend beyond the immediate/acute time period after the injury. For a professional to employ this diagnosis the following criteria are required: There are organic (physical) and psychogenic (psychological) disturbances observed after closed head injury. There are problems with this diagnosis. To begin with, the definition of “organic” is unclear, plus it is an obsolete non-specific term referring to syndromes arising from brain disease (Loring and Meador, 1999)²¹. Neuropsychologists can measure deficits in cognitive functioning but establishing a relationship between the deficits and their source of brain disease (i.e. organicity) is extremely difficult unless there is unequivocal evidence of brain damage found in neuroradiological studies of patients who have suffered strokes, complicated-mild traumatic brain injuries, or moderate/severe brain injuries.

Because the PCS is attributed to concussions, as opposed to significant brain damage, current brain scanning techniques are not sensitive to so-called organicity. Thus, trying to determine whether an abnormal brain scan is causally related to a concussion and/or cognitive deficits is compromised since many patients without concussions or cognitive deficits have abnormal brain scans (Evans, 2017)²². There are also patients with normal scans that have significant cognitive deficits measured by neuropsychological tests (Decobert, 2005)²³. Finally, there are cases where normal CT and normal cognitive functioning exists who have had concussions (Hughes et al, 2004)²⁴. Collectively, this undermines confidence in a reliable metric between distal concussion history and “organic disturbances” measured by brain scanning, at any time, or neuropsychological testing extended beyond the immediate/acute phase following the concussion. PCS includes subjective physical complaints (headaches, dizziness), psychological (emotional and behavioral changes) and cognitive changes. These disturbances can be chronic, permanent or late-emerging.

Unfortunately, the diagnosis additionally does not take into account potential fabricating (malingering) or magnification of reporting collectively in the service of achieving a specific goal (Rogers and Bender, 2013)¹⁶. Thus, the PCS diagnosis made without empirical evidence (neuropsychological examination) to support valid patient complaints will introduce questionable clinical data (Larrabee, 2012)¹⁷. The literature is replete with studies of intentional deceptive reporting gained through unstructured clinical judgment and validity tests revealing high rates of invalid neuropsychological information: 38.5% (Larrabee, 2003)¹⁹, 58% (Armistead-Jehle, 2010)¹⁸, and 30% (Young, 2015)²⁰ are just some examples.

Finally, physical, psychological, and cognitive symptoms are not specific to concussion (Larrabee, 2012)²⁵ ,and if they are, they must occur more often among these patients than among those without the diagnosis (Faust and Ahern, 2012)²⁶. To rephrase, there is an associative correlation made by the patient between their symptoms and their concussion whereby these symptoms are misattributed to the index trauma. Without all the facts-frequency of the symptoms when the disorder is present and when it is not present, the determination cannot be made. This is known as analysis of covariation (Faust and Ahern, 2012)²⁷. This expands the source for PCS into alternative differential considerations, besides mitigating defence exposure when responsible for causation.

Alternative Causes Manifesting as Post-Concussion Syndrome

Before accepting the concussion and post-concussion diagnoses at face value, the following are potential sources that can account for ongoing symptoms: posttraumatic stress disorder (Flynn, 2010)²⁸, orthopedic injuries (Mickeviciene et al, 2004)²⁹, whiplash (Sullivan et al, 2002)³⁰, chronic pain (Iverson and McCracken, 1997)³¹, outpatient treatment due to psychological problems (Fox et al, 1995)³², pre-injury personality disorders (Hibbard et al, 2000)³³, anxiety (Meares et al, 2011)³⁴, depression (Basso et al, 2013)³⁵, the manner in which symptoms are elicited from the patient (Iverson et al, 2010)³⁶, and finally litigation (Lees-Haley & Brown, 1993)³⁷.

How Common Is the Post-Concussion Syndrome?

The rate at which a diagnosis occurs is known as the base rate, and in turn, it determines the likelihood of a clinician correctly diagnosing the condition. The base rate for PCS is not known with certainty because not all patients who incur a concussion report it to doctors (Sosin et al, 1996)³⁸. Many researchers have concluded different base rates and I shall only reference the leaders since there are too many to list. McCrea (2008)³⁹ reported a base rate for PCS of 1 to 5%. Larrabee (2005)⁴⁰ concluded a single uncomplicated mild traumatic brain injury with neuropsychological deficits persisting for up to three months, but the norm is full recovery, with no long-term residual deficits. There is increasing evidence that questions the validity of the PCS symptom constellation. To qualify as a syndrome, a condition must demonstrate a set of specifically associated symptoms broadly present in persons who have the condition and absent those who do not have it.

There is increasing evidence that questions the validity of the PCS symptom constellation.

In summary, current research has definitively demonstrated that a patient with an MTBI has no long-term cognitive or psychological deficits. This is supported by the Committee on Traumatic Brain Injury Board on Health Care Services (Institute of Medicine, 2006)⁴¹, the American Medical Association (Giza et al., 2013)⁴², and 6 meta-analyses representing hundreds of studies (Rohling et al, 2017)⁴³.

If Not Post-Concussion Syndrome, What Is the Diagnosis?

PCS is a condition in search of a specific cause. Adjustment disorder, posttraumatic reaction or post-accident syndrome/post-injury syndrome (Bush & Myers, 2013)⁴⁴ are more appropriate diagnoses since they include the amalgam of physical, psychological and cognitive symptoms secondary to accidents that include concussion. Until PCS can be casually related to concussion in a reliable way, it is more appropriate for clinicians to not diagnose PCS – particularly those working in a legal setting – and alternatively consider the aforementioned conditions underscoring the persistent symptoms.

Strategic Considerations: Defence of Post-Concussion Syndrome Claims

When preparing for the defense of PCS cases, I believe they should be divided into two groups:

1. Those in which the PCS diagnosis or the plaintiff’s theory of causation is plainly wrong, and:
2. Those in which the plaintiff is substantially correct – neuropsychological damages, largely the result of defendant’s actions, are present – but there exists another side to the story, complexities the plaintiff glosses over; in short, mitigating data important to the defence and to which the trier of fact is entitled. When the defendant’s actions do indeed result in the PCS, of course, the ethical defendant does not simply deny the plaintiff’s claims. However, pre-injury conditions considered earlier in this article would reasonably limit the defense exposure to just that proportionate to damages caused by the defendant.

Defence of the PCS is found in one or more of three areas:

1. The index trauma was neither one a reasonable person would experience as traumatic nor likely to trigger a disabling PCS. The defence should be alert to situations in which the plaintiff has actually fully recovered from a painful injury and the persistent cognitive changes attributed to defendant’s actions now instead result from displacement and misattribution from other concurrent but unrelated situations (Yochelson, 1975)⁴⁵.
2. The principal injury, though authentic and demonstrable, is clinically trivial. There is good evidence for an inverse dose-response effect in litigated neurological injury: The more minor the neurological injury, the greater the likelihood of response distortion (Green, Iverson, & Allen, 1999)⁴⁶.
3. The symptoms and condition of which the claimant complains were preexisting. If the claimant’s PCS symptoms are disproportionate to the alleged trauma, a clinical inquiry will reveal the claimant had long suffered disabling cognitive and psychological symptoms now being laid in their entirety at the feet of the trauma. In fact, the more severe the reaction the more likely the claimant had been struggling for years with that for which he/she now seeks compensation. Thus, the claimant’s PCS reflects less an acute, secondary neuropsychological injury than a longstanding personality disorder referenced earlier in terms of preexisting psychological disequilibrium.

Essential Factors in the Assessment of the Post-Concussion Syndrome Claimant

Neuropsychological examination (NPE) is especially useful in PCS and brain injury cases (Sica, 2017)⁴⁷. The NPE enable cognitive and psychological determinations to be made. The appropriate approach to this diagnosis relies on a multi-method convergent means of data gathering. Three recommended overlapping methods of NPE are: review of outside records (e.g. CT, MRI, depositions) and consultation with observation and neuropsychological, forensic, and psychological test scores (Lally, 2003)²⁴. Lally refers to these three evidentiary sources as the “tripod” on which neuropsychological testimony rests, and further argues that this approach places a neuropsychologist at an advantage over other mental health professionals. This is particularly elaborated upon by Sica (2020) in terms of the unique position of neuropsychology in the clinical and legal setting.

Conclusions

Presently, research has brought us to the point where distinctions between MTBIs, complicated-mild TBIs, moderate TBIs and severe TBIs can be made. Attorneys and clinicians involved with concussions (MTBI) and PCS need to know the definitional distinctions and that it is impeachable for reasons discussed in the body of this article. Also, the fact that research indicates the base rate for PCS is extremely low, and thus, legal challenges can justifiably be raised when this questionable diagnosis is made with reasonable medical certainty.

The definitional evolution of traumatic brain has come a long way, providing clarity regarding the PCS diagnosis and thereby providing the fact finder a just legal outcome. May this article be the requiem for the PCS diagnosis. I rest my case.

REFERENCES

¹ Bazarian, J. J., McClung, J., Shah, M. N., Cheng, Y. T., Flesher, W., and Kraus, J. (2005). Mild Traumatic Brain Injury in the United States, 1998-2000. The journal is Brain Injury, 19, 85-91.

² Ruff, R. M., Iverson, G. L., Barth, J. T., Bush, S. S., and Broschek, D. K. (2009). Recommendations for Diagnosing a Mild Traumatic Brain Injury. A National Academy of Neuropsychology Education Paper. Archives of Clinical Neuropsychology, 24, 3-10.

³a) Ruff, R. M., and Richardson, A. M. (1999). Mild Traumatic Brain Injury in J. Sweet (Ed.), Forensic Neuropsychology: Fundamentals and Practice (pp. 315-338). Amsterdam, The Netherlands: Swets and Zeitlinger.

b) Sweet, J. J., and Meyers, D. G. (2012). Trends in Forensic Practice and Research. In G. J. Larrabee (Ed.), Forensic Neuropsychology: Scientific Approach (2^nd, pp. 501-519). New York, NY: Oxford University Press.

⁴G. Larrabee (Ed.), Forensic Neuropsychology: Scientific Approach (PP: 209-236), New York: Oxford University Press.

⁵Lishman, W. A., The Psychiatric Sequelae of Head Injury, Psychological Medicine, 1973 August: 3 (3): 304-18.

⁶ Symonds, C. P., Mental Disorder Following Head Injury

Proc R SOC MED, 1937 July; 30 (9); 1081-94.

⁷O’Donnel, M. L. Psychiatric Morbidity Following Injury, American Journal of Psychiatry, 2004 March; 161 (3): 507-14.

⁸Fann, W. E. and Sussex, J. N., Late Effects of Early Dependency Need Deprivation: Meal Ticket Syndrome, British Journal of Psychiatry, 1976 March 128: 262-8.

⁹Gunstad, J. and Suhr, J. A. (2004) Cognitive Factors in Post-Concussion Syndrome Symptom Report. Archives of Clinical Neuropsychology, 19, 391-405.

¹⁰Alexander, M. P. (1995) Mild Traumatic Brain Injury: Pathophysiology, Natural History, and Clinical Management. Neurology 45; 1253-60.

¹¹Ruff, R. M., Iverson, G. L., Barth, J. T., Bush, S. S., and Broschek, D. K. (2009). Recommendations for Diagnosing a Mild Traumatic Brain Injury. A National Academy of Neuropsychology Education Paper. Archives of Clinical Neuropsychology, 24, 3-10.

¹²Uzzell, D. (1999). Mild Head Injury: Much Ado About Something. In N. R. Varney and R. J. Roberts (Eds.). The Evaluation and Treatment of Mild Traumatic Brain Injury (pp. 13-26). Mahwah: Lawrence Erlbaum Associates.

¹³a) Binder, L. L. M. (1997). Review of Mild Head Trauma. Part II: Clinical Implications, Journal of Clinical and Experimental Neuropsychology, 19, 432-457.

b) Larrabee, G. J. (1999). In N. R. Varney and R. J. Roberts (Eds.). The Evaluation and Treatment of Mild Traumatic Brain Injury Current Controversies a Mild Head Injury: Scientific and Methodologic Considerations (PP. 327-345). Mahwah: Lawrence Erlbaum Associates Publishers.

¹⁴Anderson-Barnes, V. C., Weeks, S. R., and Tsao, J. W. (2010). Mild traumatic brain injury updates. CONTINUUM: Lifelong Learning in Neurology, 16, 17-26.

¹⁵Goodheart, C. D. (2014). Primer for ICD-9-10-CM Users: Psychological and Behavioral Conditions. Washington, DC: American Psychological Association.

¹⁶Roger, R., and Bender, S. (2013). Evaluation of Malingering and Related Response Styles. In A. M. Goldstein (Ed.), Handbook of Psychology: II (Forensic Psychology) (pp. 517-540). Hoboken: John Wiley and Sons, Inc.

¹⁷Larrabee, G. J. (2012). Performance Validity and Symptom Validity in Neuropsychological Assessment. Journal of the International Neuropsychological Society, 18, 625-630.

¹⁸Armistead-Jehle, P. (2010). Symptom Validity Test Performances in US Veterans Referred for Evaluation of Mild TBI. Applied Neuropsychology, 17 (1), 52-59.

¹⁹Larrabee, G. J. (2003). Detection of Malingering Using Atypical Performance Patterns on Standard Neuropsychological Tests. The Clinical Neuropsychologist, 17 (3), 410-425.

²⁰Young, G. (2015). Malingering in Forensic Disability Related Assessments: Prevalence 15± 15%. Psychological Injury and Law, A (3), 188-199.

²¹Loring, D. W., and Meador K. J. (1999). INS Dictionary of Neuropsychology, Oxford University Press.

²²Evans, R. W. (2017). Incidental Findings and Normal Anatomical Variants on MRI of the Brain in Adults for Primary Headaches. Headache: The Journal of Head and Face Pain, 57, 780-89.

²³Decobert, F. (2005). Unexplained Mental Retardation: Is Brain MRI Useful? Pediatric Radiology, 35, 587-596.

²⁴Hughes, D. G., Jackson, A., Mason, D. L., Berry, E., Hollis, S., and Yates, D. W. (2004). Abnormalities on Magnetic Resonance Imaging Seen Acutely Following Mild Traumatic Brain Injury: Correlation with Neuropsychological Tests and Delayed Recovery. Neuroradiology, 46, 550-558.

²⁵Larrabee, G. J. (2012). Performance Validity and Symptom Validity in Neuropsychological Assessment. Journal of the International Neuropsychological Society, 18, 625-630. (2012)

²⁶Faust, D., & Ahern, D. C. (2012). Clinical Judgment and Prediction. In D. Faust (Ed.), Coping with Psychiatric and Psychological Testimony (6^th Ed., PP. 147-208). New York: Oxford University Press.

²⁷Faust, D, & Ahern, D C (2012). Clinical Judgment and Prediction. In D Faust (Ed), Coping with Psychiatric and Psychological Testimony (6^th Ed., PP. 147-208). New York: Oxford University Press.

²⁸Flynn, F G (2010). Memory Impairment After Mild Traumatic Brain Injury. CONTINUUM: Lifelong Learning in Neurology, 16, 79-109

²⁹Mickeviciene, D, Schrader, H, Obelieniene, D, Surkiene, D, Kunickas, R, Stovner, L, and Sand, T (2004). A Controlled Prospective Inception Cohort Study on the Postconcussion Syndrome Outside The Medicolegal Context. European Journal of Neurology, II, 411-419.

³⁰Sullivan, M J, Hall, E, Bartolacci, R, Sullivan, M E, and Adams, H (2002). Perceived Cognitive Deficits, Emotional Distress and Disability Following Whiplash Injury. Pain Research and Management, 7, 120-126.

³¹Iverson, G L, & McCracken, L M (1997), Postconcussive Symptoms in Persons with Chronic Pain. Brain Injury, II, 783-790.

³²Fox, D D, Lees-Haley, P R, Earnest, K, and Dolezal-Wood, S (1995). Base Rates of Postconcussive Symptoms in Health Maintenance Organization Patients and Controls. Neuropsychology, 9, 606-611.

³³Hibbard, M R, Bogdany, J, Uysal, S, Kepler, K, Silver, J M, Gordon, W A, and Haddad, L (2000). Axis II Psychopathology in Individuals with Traumatic Brain Injury. Brain Injury, 14, 45-61.

³⁴Meares, S, Shores, E A, Taylor, A J, Batchelor, J, and Bryant, R A (2011). The Prospective Course of Postconcussion Syndrome: The Role of Mild Traumatic Brain Injury. Neuropsychology, 25, 454-465.

³⁵Basso, M, Miller, A, Estevis, E, and Combs, D (2013). Neuropsychological Deficits in Major Depressive Disorder: Correlates and Conundrums. In P A Arnett (Ed), Secondary Influences on Neuropsychological Test Performance (PP. 39-66), New York: Oxford University Press.

³⁶Iverson, G L, Brooks, B L, Ashton, V L, and Lange, R T (2010). Interview Versus Questionnaire Symptom Reporting in People with the Postconcussion Syndrome. The Journal of Head Trauma Rehabilitation, 25, 23-30.

³⁷Lees-Haley, P R, & Brown, R S (1993). Neuropsychological Complaint Based Rates of a 170 Personal Injury Claimants. Archives of Clinical Neuropsychology, 8, 203-209.

³⁸Sosin, D M, Sniezek, J E, and Thurman, D J (1996). Incidence of Mild to Moderate Brain Injury in the United States, 1991. Brain Injury, 10, 47-54.

³⁹McCrea, M (2008). Mild Traumatic Brain Injury and Postconcussion Syndrome: The New Evidence Base for Diagnosis and Treatment. New York: Oxford University Press.

⁴⁰Larrabee, G (2005). Mild Traumatic Brain Injury. In G. Larrabee (Ed), Forensic Neuropsychology: Scientific Approach (PP. 209-236), New York: Oxford University Press.

⁴¹Institute of Medicine (2006). Evaluating the HRSA Traumatic Brain Injury Program. Washington, DC: National Academic Press.

⁴²Giza, C C, Kutcher, J S, Gioia, G A, et al., (2013). Summary of Evidence-Based Guideline Update: Evaluation and Management of Concussion in Sports: Report of the Guideline Development Subcommittee of American Academy of Neurology. Neurology, 80, 2250-2257.

⁴³Rohling, M, and Axelrod, B (2017). Mild Traumatic Brain Injury. In S S Bush, G J Demakis, and M L Rohling (Eds), ATA Handbook of Forensic Neuropsychology (pp. 147-200). Washington, DC: American Psychological Association.

⁴⁴Bush, S S, & Myers, T E (2013). Neuropsychological Services Following Motor Vehicle Collisions. Psychological Injury and Law, 6, 3-20.

⁴⁵Yochelson, L, Traumatic Neurosis, Readings in Law in Psychiatry, Ed. R C Allen, E Z Ferster, and J G Rubin (Johns Hopkins University Press, 1975).

⁴⁶Green, P, Iverson, G L, & Allen, L (1999), Detecting Malingering in Head Injury Litigation with the Word Memory Test. Brain Injury, 13, A13-9.

⁴⁷Sica, R B (2017) Neuropsychological Observations, Clinical Judgement, Objective Evidence and Their Variable Applications. Psychological Innovations, Vol. 2, No. 1, 21-26.Sica, R B (2020) Medical Adjustment Counseling: An Evidence-Based Neuropsychological Approach in the Care of Medical Patient, Neuro Rehabilitation, 46, 213-225.

⁴⁸Lally, S J (2003). What Tests are Acceptable for use in Forensic Evaluations? A Survey of Experts. Professional Psychology: Research and Practice, 34, 491-98.

 

Dr Robert B Sica, PhD, ABN, FACPN

Board-Certified In Neuropsychology # 84, #255

Director, Principal, Neuropsychological Rehabilitation Services | LifeSpan

Fellowship Residency Supervisor

Jersey Shore University Medical Center, Neuroscience Division

Clinical Assistant Professor, Rutgers-Robert Wood Johnson Medical School

Clinical Assistant Professor, Seton Hall – Hackensack Meridian School of Medicine

 

NRS|LS

Address: 2100 Route 33, Suite 9-10, Neptune, NJ 07753

Telephone: (732) 988 3441

Fax: (732) 988 7123

Email: rsica18@hotmail.com

 

Neuropsychology Rehabilitation Services – LifeSpan (NRS|LS) was founded in the late 1970s. It is a joint practice consisting of a neuropsychological rehabilitation program, a multi-specialty health psychology program and a behavioural health program treating a variety of mental health conditions.  The practice also treats the full spectrum of brain conditions, including but not limited to concussion, traumatic brain injuries, cerebrovascular accidents, brain tumours, dementia and learning disabilities.  Finally, the practice is involved with pharmaceutical clinical trials for children and adults. NRS|LS is affiliated with Hackensack Meridian Health, Jersey Shore University Medical Center Neuroscience Division, and is staffed by licensed neuropsychologists and other healthcare experts.

Dr Robert B Sica is the originator, principal and director of NRS|LS and has lectured and published in neuropsychology and forensic neuropsychology, drawing upon over 40 years of clinical experience in private practice, hospital, academia, and law. He was the first clinical neuropsychologist on staff at Jersey Shore University Medical Center, Neuroscience Division, and Riverview Medical Center, both hospitals part of Hackensack Meridian Health, where he treats patients along with academic responsibilities teaching medical students and neuropsychological fellows.  He is a clinical assistant professor at both Rutgers-Robert Wood Johnson Medical School and Seton Hall – Hackensack Meridian School of Medicine.  Finally, he was a managing partner in the development of the Jersey Shore University Medical Arts Center building, a joint venture between staff physicians and the hospital. He holds a PhD in psychology and was a key leader in the 1970s brain injury rehabilitation movement.