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Triple Optics - Dilated Peoples - The Platform (CD, Album)

10.01.2022

From beauty to pain and release, and often back again, each track and not in a bad way seems open-ended; a constant flowing cycle of emotions, which can be healed during that moment, in that space and time, but will inevitably return: A calm followed by turbulence and hopefully the light. The rest of H.

Anguish has seldom sounded sweeter. Photo credit: Caio Ferreira. Holding up his guitar like some sort of offering, or a transmitter to the sky, Gat stands as a vessel for a cerebral multilayering of musical influences.

National Conservatory and living amongst the Czech exiles in the desired haven state of Iowa, this New World Symphony as he called it, is included for its own embrace of Native Indian culture, the Irish immigrants folk songs and the music of the misfortunate African slaves. Billed as a very different kind of Black Light White Light album, Ejlersten going as far as strongly considering releasing it under an entirely separate project moniker, the horizons explored and discovered on this record prove very fruitful indeed.

A Western adventure of melancholic beauty, the debut album from The Magic City Trio treads familiar ground as it pays homage to a century and more of the frontier spirit and tragedy. Liltingly duets in the manner of an imagined partnership between Lee Hazlewood and Emmylou Harris feature throughout, whilst hints are made to The Flying Burrito Brothers one minute and a lonesome pinning Richard Hawley on the ranch, the next. Missing out on scoring the golden age of Westerns then, The Magic City Trio which expands to accommodate a number of guests walk the walk, talk the talk, but update the old tropes for a post-modernist take.

It sounds like an unforgiving vision as re-imagined by a 70s period Scott Walker, earmarked for a revisionist Tarantino Western. Far more than a pastiche or mere homage, Amerikana Arkana is a subtly attuned to modern sensibilities version of a lost classical Western soundtrack: a most diaphanous and sweetly lamentable one at that. One of their latest reissues is the amorphous experiment between extemporized music and op art Mouvements. This Geneva underground scene missive was originally released as a private box set, limited to only copies and sold at art galleries.

Instigated by the guitar player though free and easy across a whole instrument spectrum Christian Oestreicher after meeting the artist and painter Richard Reimann at the Aurora art gallery in Geneva, the Mouvements project emulated what was an already flourishing scene of cross-pollinated arts. Oestreicher on his part, attempted a process of reification through a mix of free-jazz, musique-concrete, psych rock, tape effects manipulation and Krautrock; Reimann would provide the reference point metallic and shimmered geometric artwork.

Sessions for the eventual album began in ; recorded at an ad hoc studio in an occupied mansion using a trio of Revox machines. A number of recurring instruments, such as the violin and guitar, return us to some sort of thematic semblance, something to follow and recognize. A spark of interest for those unfamiliar with the Swiss branch of the art-rock crossover in the early 70s, this most intriguing artifact from the period focuses on a hitherto forgotten, or at least passed over, development in the story of European avant-garde; a time when Op Art and free-music experimentation collided.

Building his own shortened, elongated and mashed-up versions of turntables and various plucked, rung or clanged instrumentation in his garden Triple Optics - Dilated Peoples - The Platform (CD, his process methods would seem almost impossible to replicate let alone repeat.

And so this often ennui shifting and dislocation of the avant-garde, techno, breakbeat and Kosmische sounds often unique. Previously causing mayhem under the — Duchampian chess move favorite — Nimzo-Indian moniker, Spackman has now adopted a new nom de plume; a home for what he intends to be, like the name suggests, the most saddest music.

Yet with a few releases already under his tool belt, the latest epic, Slow Birdis more an exploration in confusion and ghostly visages of the cosmos than a melancholic display of plaintive moping. There are by all means some moody, even ominous, leviathans lurking and the odd daemonic vocal effect, but as with most of the tracks on this LP they constantly evolve from one idea into the next: anything from a panic attack to the kooky.

The title track itself certainly features flighty and rapid wing flapping motions, yet rubs against more coarse machinery, knife sharpening percussive elements and Forbidden Planet eeriness.

Parrot by comparison, sounds like an inverted PiL, languidly reversed to the undulations of bongos, whilst Sparrow pairs Cecil Taylor piano serialism with, what sounds like, a wooden ball rolling across a tabletop. A cacophony of clever layering and ever-changing focus takes tubular metallics, UNCLE drum break barrages, Ippu Mitsui, Add N To Xgiddy oscillations, haywire computer and staccato phonetic languages, Vader mask style breathing, glints of light beams, the Aphex Twin on xylophone and produces his own, whatever that is, niche of electronic composition.

It can feel a slog and overwhelming at times, but Slow Bird is one of his most progressive and well-produced releases yet; mayhem at its best. Battling to overcome the mentally and physical debilitations of anxiety disorder, the artist who I only know as John behind this new solo project, Evil Boneseeks a reification of its enervated effects on the soporific, halcyon In Vain.

The title, a quite resigned one, refers to his attempts to beat it: all to no effect. Though, as John candidly muses, it is now a part of his make up, and in many ways impacts on the music he creates. Despite often stifling creativity, the first track from Evil Bone is a haze of languid shoegaze and soulful dream pop that recalls Slowdive and The Cocteau Twins cloud bursting in vaporous anguish.

Promising an extended release later in the year, In Vain sets the marker for beautifully layered anxious psychedelic pop. Though his image is plastered or is it! Mysterious then, unsettled, the experimental electronic music with textured industrial and squalling rock guitar style of sonic noodling Hillary produces is more akin to an amorphous collection of soundtracks than identifiable song material.

Evocations, moods, setting the scene for some futuristic heart of darkness, Hillary fashions a gunship waltz of tetchy synthesized percussion, fairground noises, whistling satellites and rocket attacks on the fantastical entitled Eamon The Destroyerwhilst on the title track, he plays around, almost plaintively, with folksy acoustic plucked notation, sighing strings, twinkly xylophone and arched electric guitar.

Yet, even with title prompts, you could be anywhere on these unique vistas and musings. Following on from the warm afterglow of their last outbound journey, Adventurethe London-based though originally hailing from Southport duo of lilted psychedelic pop once more dip liberally into the 60s and early 70s songbook on their fourth album, Stuck In A Daydream.

Suffused with their hazy recondite influences throughout, they channel Jimmy Campbell, Badfinger, Bread and Let It Be era Beatles alone on the first yearning and rolling piano glorious pop song, Consider Me.

Later on we hear lullaby twinkled mobiles that hang over daydreamers in the style of Fairfield Parlour; the sea shanty whimsy lament of a lovesick merman as fashioned by The Kinks; troubled relationships as re-imagined by an art philistine metaphorical Rubber Soul era George Harrison; and a sad eulogy to an absent friend as plaintively sung by Gram Parsons. However, its age old themes speak volumes about the here and now, offering shelter and an antidote to these tumultuous times; those gilded metaphors speaking volumes about the here and now.

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At the end of this chapter a list of textbooks that provide in-depth review of these disorders can be found. Non-progressive motor impairment as a result of insult to the developing brain, usually within the first two years of life, is known as cerebral palsy and is discussed in Chapter The poor motor performance may manifest as coordination problems, poor balance, clumsiness, dropping or bumping into things; marked delays in achieving developmental motor milestones e.

C The disturbance is not due to a general medical condition e. These difficulties may be associated with learning, attention and social interaction difficulties.

The history often reveals delay in acquisition of motor milestones and early awkwardness in motor coordination, and there may be a family history of similar motor difficulties. The clinician needs to ask about delayed walking or progressive weakness in a family member, which could indicate an inherited neuromuscular disorder.

Children with DCD show delay or difficulties with their gross and fine motor skills, but should have an otherwise normal neurological examination including normal muscle strength and reflexes. These children can have poor self-esteem and may be the victims of bullying. The result is that they withdraw from such activities, spend time in the school library during school breaks and display reluctance in attending school sport. Social and emotional difficulties also persist and may worsen.

Also, if the child has not had the opportunity to experience physical activities that enhance the development of motor skills, for reasons unrelated to a developmental problem, the child will be less able at physical tasks than his more experienced peers. Central involving the brain and spinal cord and peripheral or neuromuscular involving anterior horn cell, peripheral nerve, neuromuscular junction or muscle disorders may cause motor delay or abnormalities with motor coordination, and a detailed history and physical examination are essential to exclude them.

A history of perinatal difficulties including fetal distress, the presentation and mode of delivery, Apgar scores and need for resuscitation and support in the neonatal period are important when considering the possibility of cerebral palsy.

The age at which various developmental milestones were achieved should be accurately documented refer to Chapter 1 and Tables 1. Children with DCD should have a normal neurological examination without weakness focal or generalisedsensory loss, spasticity, cranial nerve abnormalities or cerebellar signs.

Excessive ligamentous laxity may indicate a connective tissue disorder. Initial evaluation for a central disorder usually includes thyroid function tests, urine metabolic screen, serum lactate, cranial and spinal imaging, karyotype and a comparative genomic hybridisation CGH array. Hypotonia and absent reflexes are indicative of a neuromuscular disorder.

The commonly occurring neuromuscular inherited disorders presenting in childhood, and the level of lesion, are indicated in Table 3. Duchenne muscular dystrophy, and is raised to a lesser extent with spinal muscular atrophy and other myopathies.

The serum creatine kinase CK is significantly raised in affected boys and may be mild to moderately raised in carrier mothers. The diagnosis is confirmed by identifying a mutation on the dystrophin gene on multiplex PCR, multiplex ligation-dependent probe amplification MLPAor sequencing. Consensus standards for the diagnosis and management of boys with DMD have recently been published.

With progression, distal weakness and wasting, foot deformity and distal sensory loss are seen. Deep tendon reflexes are absent or reduced on examination. In children with Duchenne muscular dystrophy, glucocorticoids prednisolone, deflazacort improve muscle strength and prolong ambulation, reduce risk of progressive scoliosis, and stabilise respiratory and cardiac function. An accurate genetic diagnosis is also becoming increasingly important for counselling about risks with future pregnancies, for screening pregnancies, and for enrolment in clinical trials.

Continued follow-up is essential to ensure that there is no progression or worsening of the motor or cognitive difficulties. Improved outcomes following early intervention for children with DCD is supported by research. Ideally the therapist works closely with the parent or carer in a family-centered manner to ensure that the family can continue the techniques used during therapy sessions at home. The OT assists with training in functional daily living skills like dressing, doing buttons and shoelaces, feeding and personal hygiene.

Some schools have therapists either on staff or visiting the school on a regular basis. Psychological support and counselling may be necessary where poor self- esteem resulting from poor motor skills, e. It also helps to find a skill that the child is good at and focus therapy and intervention to develop that skill in order to improve self-esteem and to encourage a sense of achievement, e.

The child who has expressive speech difficulty verbal dyspraxia needs early referral to a speech and language therapist for targeted intervention. See Chapters 6 and 8. Approaches to intervention Modern intervention for DCD fits into one of two approaches. This approach was updated and renamed Ecological Intervention EI. EI places emphasis on actual control of movement and aims to provide intervention in a family and community setting.

Hence the approach is goal orientated and child centred. Children of different ages have varied skills and ability, and there is a broad range of ability in typically developing, healthy children. Developmental Coordination Disorder. Children with developmental coordination disorders. In: Accardo PJ, editor. Attention deficits in children and adults. New York: Marcel Decker; Developmental coordination disorder in geographic cohorts of 8-year-old children born extremely preterm or extremely low birth weight in the s.

Fine and gross motor ability in males with ADHD. ADHD and poor motor performance from a family genetic perspective. Developmental coordination disorder in Swedish 7-year-old children. Motor coordination, empathy and social behaviour in school-aged children. Motor coordination and emotional—behavioral problems in children. Current Opinion in Psychiatry ;23 4 —9 13 Cairney J. Gross motor problems and psychiatry disorders in children.

Current approaches to intervention with developmental coordination disorder. The relationship between bullying and self-worth in children with movement coordination problems.

Clumsiness in children — do they grow out of it? A year follow-up study. Are impaired childhood motor skills a risk factor for adolescent anxiety?

Am J Psychiatry ;—5 18 Sewry C. Muscular dystrophies: an update on pathology and diagnosis. Congenital myopathies. Muscle MRI in inherited neuromuscular disorders: past, present, and future. Electrodiagnosis of polyneuropathy. Limb—girdle and congenital muscular dystrophies: current diagnostics, management, and emerging technologies. Failure of early diagnosis in symptomatic Duchenne muscular dystrophy.

Diagnosis and management of Duchenne muscular dystrophy, Part 1: diagnosis, and pharmacological and psychosocial management. Diagnosis, natural history, and management of Charcot-Marie- Tooth disease. Hereditary motor and sensory neuropathies. Peripheral Neuropathy. Philadelphia: WB Saunders; Neurology ;64 1 —20 29 Jeste SS.

The neurology of autism spectrum disorders. Motor and perceptual—motor competence in children with Down syndrome: variation in performance with age. Cognitive strategies and motor performance in children with developmental coordination disorder. Intervention approaches and children with developmental coordination disorder. Pediatric Rehabilitation ;—47 33 Ayres AJ.

Sensory Integration and the Child. Approaches to assessment and treatment of children with DCD: an evaluative review. Enabling occupation in children. Clumsy children. British Medical J ;—6 Developmental coordination disorder.

Movement disorders, ch 9. In: David RB, editor. Pediatric Neurology for the Clinician. Neurophysiologic Basis for the Treatment of Movement Disorders, ch Developmental Disabilities in Infancy and Childhood. A fourth type of loss, auditory neuropathy, has emerged as a distinct entity over the past decade. Auditory neuropathy spectrum disorder ANSD is a disorder of hearing in which cochlear function is essentially spared while auditory nerve activation is impaired.

Children with ANSD may have speech perception and word discrimination problems that are disproportionate to their hearing thresholds. Many deaf people do not regard their condition as a handicap, but rather as a part of their identity. The National Health and Nutri- tional Examination Survey NHANES that used formal audiologic evaluation and included even very mild measured degrees of hearing loss, including isolated low and high frequency losses, gave an estimated prevalence of Aetiology of hearing loss remains unknown in 35—55 per cent of most reported case series.

Sensorineural hearing loss Genetics About 70 per cent of genetically determined hearing loss occurs without other clinical abnormalities, i. Most newborns with inherited forms of hearing loss are born to hearing parents and have recessive, non-syndromic losses. Some genes have been identified that are associated with both dominant and recessive non-syndromic deafness, and also with both syndro- mic and non-syndromic deafness, emphasising the complexity of this fast-growing field and the difficulties inherent in providing accurate genetic counselling.

A number of deafness-associated pigmentary disorders are caused by mutations in genes that in some way regulate MITF expression or activity. Recessive mutations in the PDS gene are the common cause of Pendred syndrome.

Mutations in the same gene can cause non-syndromic hearing loss associated with temporal bone abnormalities, which cross the spectrum from isolated enlargement of the vestibular aqueduct EVA to Mondini dysplasia. These temporal bone abnormalities may be caused by a side-splice mutation in the PDS gene. Consanguinity of the parents or an affected sibling might suggest an AR aetiology. In the absence of any other apparent aetiology, some authors estimate that the likelihood for an AR aetiology of hearing loss may be as high as 80 per cent.

Recessive mutations at a single locus, GJB2 or Connexin 26, are now thought to account for more than half of all genetic cases of deafness in some, but not all, populations. Hearing loss due to Connexin 26 mutations can vary from mild to profound, even within the same sibship, and is non-syndromic, accompanied by normal vision, vestibular responses, and no malformations of the inner ear detectable by CT scanning.

Progressive and asymmetrical hearing loss has been noted, but accounts for less than one-third of cases. Digenic interactions are an important cause of deafness in individuals who carry a single mutation of the Connexin 26 locus together with a deletion involving the functionally related Connexin 30 locus. Connexins are the building blocks of gap junctions with six connexins oligomerising to form a hexa- meric torus called a connexon.

Most forms of AR non-syndromic hearing impairment cause a prelingual hearing loss, generally severe—profound, and not associated with any radiological abnormality. Affected males usually eventually require kidney transplantation. Hetero- zygous females have widely varying outcomes, with some having normal urinalysis and kidney function, while others develop deafness and ESRD. The variation in females may be due in part to skewing of X-chromosome inactivation.

Some are associated with systemic neuromuscular disorders, such as Kearns—Sayer syndrome, while others are associated with non- syndromic hearing loss. One specific mutation, AG, is associated with predisposition to aminoglycoside toxicity and hearing loss.

Although mutation screening in this gene has been recommended prior to aminoglycoside use as a preventive strategy, in practice the mutation does not occur with sufficiently high frequency in the population to justify this approach. Presence of the mutation alone, even in the absence of aminoglycoside exposure, may result in sensorineural hearing loss.

Both condi- tions are sporadic, with a female preponderance. These are generally categorised as prenatal, perinatal and postnatal causes. Prenatal Maternal infections including rubella, toxoplasmosis, cytomegalovirus CMVsyphilis, herpes and AIDS are all associated with development of hearing loss in the fetus.

Although prenatal ototoxic drug exposures, e. The audiologic phenotypes associated with many genes overlap, while some syndromes have variable penetrance of phenotypic features, making the distinction between syndromic and non-syndromic hearing loss challenging, especially in infancy and early childhood. Testing for individual genes associated with non-syndromic hearing loss, with the exception of Connexin 26, is generally expensive and of relatively low yield, but advances in DNA sequencing are changing this picture.

It is likely that in the next decade it will become possible to identify aetiology in almost all cases of genetic deafness. Consequently caution is advised in ascribing maternal drug ingestion as a cause of childhood hearing loss. Rubella The fetus is most susceptible to the effects of the virus during the first trimester, when maternal infection is thought to result in damage to the fetus in over 20 per cent of cases.

Although congenital rubella syndrome CRS is now rare in developed countries that have efficient vaccination programs, it remains common in developing countries where such programs are lacking.

Recently experts have expressed concern that congenital rubella may undergo a resurgence due to refusal of the MMR vaccine among some population subgroups.

Although retrospective diagnosis of congenital rubella has been attempted using lymphocyte responsiveness in combination with serological testing, these techniques remain controversial and are not widely used.

Toxoplasmosis Maternal infection with toxoplasmosis is frequently mild and unnoticed. Pregnant women who have cats as house pets are at increased risk of infection and should avoid cleaning cat litter boxes. Raw meat is another potential source of infection. Up to half of affected infants are born prematurely.

Signs of infection include hepatosplenomegaly, eye damage, cerebral calcifications, macrocephaly and petechiae. Although congenital toxoplasmosis has been associated with hearing loss, prevalence of SNHL varies from 0—28 per cent in reported studies, at least in part related to treatment. Children receiving limited or no treatment have a 28 per cent prevalence of hearing loss, those in whom treatment started after age 2.

Up to 90 per cent congenital CMV infections remain undetected in the newborn period. SNHL occurs in about 35 per cent of symp- Triple Optics - Dilated Peoples - The Platform (CD newborns, who may present with retinitis, hepatosplenomagealy, petechiae and microcephaly, and in about 10 per cent of asymptomatic infected newborns.

CMV-associated hearing loss is often progressive, so any child with proven CMV requires close audiologic follow-up, even if initial hearing tests are normal. Both primary and secondary maternal infections are reported to be associated with CNS disturbances, including deafness. Recently, real-time polymerase chain reaction PCR assays of saliva specimens have been shown to be highly sensitive and specific for detection of CMV infection, offering a potential screening tool for CMV in newborns.

Although the precise factors accounting for this increased risk have not been well delineated, the following are recognised associations with SNHL. Hyperbilirubinemia Historical evidence suggests an association between very high bilirubin levels and hearing loss. There is considerable debate, which remains unresolved, about the need for aggressive treatment of neonatal jaundice in term babies without hemolysis. Some experts regard the risks of bilirubin toxicity in this group as low and aggressive treatment Triple Optics - Dilated Peoples - The Platform (CD, while others argue that sequelae such as hearing loss are presently low due to the aggressive management — phototherapy together with exchange transfusion if required — currently employed, and that there is little justification for a change in approach.

Hyperbilirubinemia has recently been associated with the clinical picture of auditory neuropathy spectrum disorder ANSD. The relationship between jaundice in the newborn period and milder degrees of hearing loss has not been well studied. Prematurity Premature infants are a vulnerable group who are exposed to a number of potential ototoxins including aminoglycosides, hypoxia and hyperbilirubinemia. Reported rates of SNHL in premature infants have varied from 1—10 per cent.

Hypoxia Chronic hypoxia is associated with hearing loss in newborns. ECMO particularly is associated with delayed onset and progressive losses. Postnatal Meningitis Meningitis is thought to account for about 6 per cent of all childhood hearing loss.

A meta-analysis of the better studies gives a 9. There are reports of hearing loss improving after meningitis, so the ideal time for defini- tive audiologic evaluation is about 4—6 weeks after the illness. Widespread use of the haemophilus influenzae B Hib vaccine, streptococcus pneumoniae Prevnar vaccine, and the newer neisseria meningitides Menactra vaccine is expected to result in a significant reduction in cases. Some children with congenital SNHL are at increased risk of developing meningitis.

Presence of the Mondini malformation, characterised by a short, flat cochlea, large vestibule, wide, Album) or missing semicircular canals, and an imma- ture sensorineural structure, is often accompanied by anomalies of the footplate of the stapes.

Sometimes cases are detected only after onset of meningitis. Ototoxins Drugs such as aminoglycosides, loop diuretics, cisplatin and salicylates have been associated with SNHL. Use of these drugs should be avoided wherever possible, especially in vulnerable populations such as premature babies. When these drugs must be used, drug levels should be monitored closely to avoid toxicity. As noted above, children with the mitochondrial mutation AG are at particular risk of aminoglycoside toxicity.

Prevalence is 15— perin the general population and is even rarer in children. This may occur as part of neurofibromatosis. Metastatic lesions causing deafness are virtually unknown in childhood. P - To The Death] [M. Sandman - Out Triple Optics - Dilated Peoples - The Platform (CD Time] [Mr. Serv-On - Life Insurance] [Mr. E - Grimey - Gods Favorite] [N.

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