And here's a more layman-like article from Scientific American: Neuronal "Superhub" Might Generate Consciousness
ETA: Found this as well (also behind an idiot wall): The effect of claustrum lesions on human consciousness and recovery of function. Abstract and snippet (and note that "LOC" means "lose of consciousness" in case that isn't clear):
Quote:
Abstract: Crick and Koch proposed that the claustrum plays a crucial role in consciousness. Their proposal was based on the structure and connectivity of the claustrum that suggested it had a role in coordinating a set of diverse brain functions. Given the few human studies investigating this claim, we decided to study the effects of claustrum lesions on consciousness in 171 combat veterans with penetrating traumatic brain injuries. Additionally, we studied the effects of claustrum lesions and loss of consciousness on long-term cognitive abilities. Claustrum damage was associated with the duration, but not frequency, of loss of consciousness, indicating that the claustrum may have an important role in regaining, but not maintaining, consciousness. Total brain volume loss, but not claustrum lesions, was associated with long-term recovery of neurobehavioral functions. Our findings constrain the current understanding of the neurobehavioral functions of the claustrum and its role in maintaining and regaining consciousness.
Crick and Koch proposed that the claustrum is the conductor of the brain’s orchestra, integrating and binding together different cortical inputs, such as color, smell, sound, and touch, into a single unifying experience in consciousness (Crick & Koch, 2005). The claustrum is a thin sheet of subcortical gray matter, separated laterally from the insula by the extreme capsule and medially from the putamen by the external capsule (Milardi et al., 2015). Although the function of the claustrum remains mysterious, its anatomical connections and cellular composition are known. The claustrum has extensive reciprocal projections, connecting the claustrum to numerous cortical and subcortical regions, such as the prefrontal cortex, primary sensory cortices, thalamus, and reticular formation (Fig. 1a) (Smith and Alloway, 2010, Torgerson et al., 2014 and Torgerson and Van Horn, 2014). Moreover, the claustrum consists of a heterogeneous mixture of cells that differ in size, shape and neurochemical composition; and single cells that possess extensive dendritic branching (Braak and Braak, 1982 and Rahman and Baizer, 2007). The structure and connectivity of the claustrum suggest that its function involves coordinating a set of diverse brain functions (Smythies et al., 2012, Smythies et al., 2014a and Smythies et al., 2014b).
Only recently, attention has been directed toward the claustrum and its possible involvement in consciousness. In a single case study, researchers demonstrated that consciousness could be immediately disrupted when the region between the insula and claustrum was electrically stimulated (Koubeissi, Bartolomei, Beltagy, & Picard, 2014). Consciousness was regained when stimulation was stopped. Moreover, stimulation in this region led to increased EEG synchrony in the medial parietal and posterior frontal regions. Nevertheless, it is difficult to generalize findings from a case study of a patient with intractable epilepsy to the general population. A second study analyzed user reports of Salvia divinorum, a psychoactive plant that contains the active ingredient salvinorin A, a κ-opioid agonist ( Stiefel, Merrifield, & Holcombe, 2014). Subjective reports described experiences of loss or altered awareness of the external environment and bodily sensations and image. Because the claustrum has a particularly high density of salvinorin A receptors, the consciousness-altering effects of S. divinorum were attributed to drug-induced disruption of the claustrum. However, salvinorin A receptors are not exclusive to the claustrum; there is also a fairly high density of receptors located in the prefrontal cortex, hippocampus, nucleus accumbens and putamen. Disruptions to other brain regions could also explain the consciousness-altering effects. It is difficult to draw conclusions about the function of the claustrum based on studies such as those reviewed above. A challenge in studying the claustrum is due partly to its poor spatial resolution in neuroimaging and the difficulty in obtaining a large sample of patients with lesions to the claustrum.
Here, we studied 171 Vietnam War veterans who sustained focal, low velocity penetrating traumatic brain injuries (pTBIs) during combat and participated in Phases 2 and 3 of the Vietnam Head Injury Study (VHIS). All patients had similar etiologies: penetrating head injuries due to bullets and shrapnel. We defined loss of consciousness (LOC) as impairments in wakefulness resulting from pTBI. Patients who experienced LOC were estimated to have Glasgow Coma Scale (GCS) scores of less than 9, which correspond with moderate or severe traumatic brain injuries (Cristofori and Levin, 2015 and Salazar et al., 1986). These patients were unable to respond to verbal commands, but may have shown some motor response by withdrawing to pain (Salazar et al., 1986). All patients participating in this study have had detailed neurobehavioral testing with well-described neurologic outcomes. To study the effect of claustrum lesions on LOC, we compared the frequency and duration of LOC experienced by patients with and without claustrum lesions. Based on previous studies that found an association between the left hemisphere and LOC (Koubeissi et al., 2014, Levin et al., 1989 and Salazar et al., 1986), we hypothesized that the left claustrum, in particular, plays a key role in consciousness. In addition, we examined the long-term effects of claustrum lesions on cognitive abilities.
Our study is the largest study to date to investigate the effects of claustrum lesions on consciousness in humans. We found that claustrum damage is moderately associated with the duration, but not the frequency, of LOC (although we did find a small effect on LOC in patients with left claustrum lesions when compared to patients without claustrum lesions). Claustrum damage was a better predictor of prolonged LOC compared to lesion size. Two other studies, as previously mentioned, have also found an association between the claustrum and LOC; they were able to either disrupt or alter consciousness using intracranial stimulation and κ-opioid agonist ( Koubeissi et al., 2014 and Stiefel et al., 2014).
We also did not find selective long-term consequences of claustrum lesions or LOC on different aspects of cognitive processing. At 35 years post-injury, patients with claustrum lesions did not exhibit long-term cognitive and language impairments after total lesion size was taken into account. Similarly, patients who had their claustrum resectioned as a result of low-grade gliomas, recovered and exhibited normal neurological examinations 3 months after having surgery (Duffau, Mandonnet, Gatignol, & Capelle, 2007); and patients who experienced uncomplicated mild traumatic brain injury (i.e., GCS scores between 13 to 15) and brief LOC did not exhibit differences in attention, learning, memory, language or executive functioning within 1 week post-injury (Iverson, Lovell, & Smith, 2000). While patients with claustrum lesions may have an increased likelihood of experiencing an extended LOC, this increased risk did not impact their ability to process the contents of consciousness when evaluated 35 years post-injury.
To which I would say from my armchair, perhaps this is due more to neural plasticity than to anything definitive about the claustrum? After all, "damage" and "lesions" evidently do not correlate and the fact that it took three months for patients to exhibit "normal neurological" functioning after having their claustrum resectioned as well as one week recovery time for "mild traumatic brain injury" argues for plasticity accounting for the brain's ability to "re-route" critical functions imho.
