Case Reports in Medicine Figure 2: There is a large area of high attenuation involving the left frontal, temporal and parietal lobes incorporating Broca’s area with subarachnoid extension and fresh haemorrhage in the suprasellar cistern. 4. Discussion Aphasia is the primary language abnormality in adults and has multiple causes including trauma, infection, brain tumours, hypoxia, and obstructive hydrocephalus. Although the association between language disorders and head trauma has been known for millenniums, descriptions of such cases were scarce until World Wars I and II, when head injuries were, for the most part, penetrating wounds [1]. In contrast with these aphasias secondary to penetrating wounds, there are still few detailed descriptions of aphasia after closed head injuries. They can be challenging clinically. The absence of signiﬁcant other neurological signs can result in cases being misdiagnosed as a transient ischemic attack or cerebrovascular accident [3]. They can be dismissed as intoxication, confusion, and psychosis or even malingering. In particular it has been noted that ﬂuent aphasia can be elusive to nonneurologically orientated physicians [4]. The availability of a neurologist allows detection of more subtle deﬁcits. The incidence of language disturbance is 1 per 1000 emergency referrals. They highlight the clinical challenge one is sometimes faced with when initially evaluating the intoxicated head injured patient. They reinforce the need to determine the mechanism of injury and thereby an appro- priately high index of suspicion. The cases presented in this paper illustrate clear examples of both motor and sensory aphasias associated with a closed head injury and provide a guide to clinicians as to the presentation, management, and prognosis of such cases. The severity of head injury can be scored on numerous parameters such as GCS on arrival, neurological deﬁcit, and/or CT ﬁndings. One of the most consistent prognostic markers used in the medical literature is the presence of post- traumatic amnesia (PTA), where PTA for longer than one week predicts a severe head injury. There has been a growing debate in the neuropsychiatric literature on the question of whether patients who sustain a blunt head injury can develop 3 symptoms of acute stress disorder (ASD) and posttraumatic stress disorder (PTSD). These are typically characterised by fear and intrusive recollections of the event. Speech deﬁcits do not tend to be a major component of these sequelae. Over the last few years there have been many publications in the ﬁeld of military medicine reporting cases of mild traumatic head injury due to blasts experiencing [5–7]. PTSD is less evident in the setting of severe head injury as described in the current series. Data disputing an association between traumatic brain injury and PTSD comes from Warden et al. among others [8]. He examined 47 patients with moderately severe TBI and found that although a minority of subjects endorsed the avoidance and autonomic arousal symptoms of PTSD, none reported any reexperiencing. A study of victims of road traﬃc accidents reached similar conclusions after ﬁnding a dearth of PTSD symptoms in a subgroup of patients who had brieﬂy lost consciousness [9]. Feinstein et al. report symptoms of PTSD in a sample of head-injured patients assessed within a couple of months of injury and stratiﬁed for severity of head injury on the basis of duration of PTA. However, when PTA extended beyond one hour, symptoms of reexperiencing the traumatic event (intrusive phenomena) and avoidant behaviour occurred signiﬁcantly less often. We need to recognize that irrespective of the mechanism involved, symptoms of PTSD may occur across the full range of head injury severity and demand our prompt attention [10]. Subtle changes in speech can also be evident. The spon- taneous speech of head injured patients can be inappropriate in length, confused, lacking informational content, and slow. Language deﬁcits may not be the sole cause for impairments in discourse. Normal discourse also requires adequate social and cognitive abilities, and these abilities are frequently impaired in closed head injured patients. The prognosis for recovery of language functioning is good but residual deﬁcits, especially in naming, may persist over many years. Subjective reports of language problems in head injured patients are not as frequent as the reports of memory problems. Aphasia associated with head injury can develop hours or even weeks after the initial precipitating event. It is most commonly associated with right blunt orbito-frontal trauma with a contre-coup left temporo-parietal injury [3, 11, 12]. This type of impact imparts a shearing force to the head which causes motion of the cerebral hemispheres within the closed cranium. Peripheral areas are more susceptible to direct impact with the cranium. Menon et al. describe their experience with 31 con- secutive patients with closed head injuries over a two-year period. The mean age was 36 years old. They demonstrated that poor outcome in relation to speech occurred more frequently in the presence of severe head injury (GCS < 8) on arrival or a prolonged comatosed state (>132 hours). Both patients in the current series had similar ages and had GCS scores of 4 and 9, respectively. Paradoxically case 1 (GCS = 4) had a better functional outcome. However, case 1 was comatosed for 72 hours while case 2 was comatosed for 168 hours perhaps explaining the diﬀering functional outcomes [13]. Overall, communication disability tends to recover well especially during the ﬁrst 6 months and to